The DOI matches its Crossref record; 157 of the 158 references it cites were found in a registry or an index; 119 of the 194 sources its claims cite were checked for support.
The AMPA Receptor Code of Synaptic Plasticity
Open accessAbstract
Changes in the properties and post-synaptic abundance of AMPA-type glutamate receptors (AMPARs) are major mechanisms underlying various forms of synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), and homeostatic scaling. The function and the trafficking of AMPARs to and from synapses is modulated by specific AMPAR GluA1-4 subunits, subunit specific protein interactors, auxiliary subunits, and post-translational modifications. Layers of regulation are added to AMPAR tetramers through these different interactions and modifications, increasing the computational power of synapses. Here we review the reliance of synaptic plasticity on AMPAR variants and propose “the AMPAR code” as a conceptual framework. The AMPAR code suggests that AMPAR variants will be predictive of the types and extent of synaptic plasticity which can occur and that a hierarchy exists such that certain AMPARs will be disproportionally recruited to synapses during LTP/homeostatic scaling-up, or removed during LTD/homeostatic scaling-down.
Overview
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Written from the paper’s full text.
TL;DR
This review proposes an “AMPAR code” in which AMPA receptor subunit composition, auxiliary subunits, protein interactions, and post-translational modifications determine the type and extent of synaptic plasticity. It synthesizes evidence that LTP, LTD, and homeostatic scaling preferentially recruit or remove distinct AMPAR variants, with GluA1/GluA2 C-tails and phosphorylation sites playing central roles.
Key findings
- The AMPAR code is framed as combinatorial: GluA1 alone has 11 known PTMs (7 phosphorylations, 2 palmitoylations, 1 S-nitrosylation, 1 ubiquitination), allowing 2^11 = 2,048 possible modified variants, with further complexity from heteromeric AMPARs and auxiliary subunits.
- LTP: the GluA1 C-tail is necessary and sufficient for hippocampal LTP in C-tail exchange mice; GluA1 S831 and S845 phosphorylation are associated with LTP, with single S831A or S845A knock-ins not impairing Schaffer collateral-CA1 LTP but the double S831A/S845A mutant impairing LTP and eliminating LTD. CP-AMPAR involvement in hippocampal LTP may be restricted to a narrow developmental window (blocked by IEM1460 in slices from 11–14-day-old mice but not 17–21-day-old mice).
- LTD: the GluA2 C-tail is necessary and sufficient for hippocampal NMDAR-dependent LTD; GluA2 S880 phosphorylation is required for cerebellar LTD; GluA1 S845 dephosphorylation is critical for hippocampal LTD, and peri-synaptic CP-AMPARs are transiently recruited during LTD induction in a PKA-dependent manner.
- Homeostatic scaling: scaling-up requires GluA1 S845 phosphorylation and is blocked in GluA1 S845A neurons, while scaling-down involves dephosphorylation of GluA1 S831/S845 and GluA2 S880/Y876 and AMPAR ubiquitination; phosphorylated GluA1 is resistant to scaling-down. In mouse cortex, ~80% of dendritic spines shrink during sleep in a multiplicative manner, while the remaining 20% appear to escape scaling-down.
Methods
- Narrative review; no primary experimental data are reported. The paper synthesizes published literature on AMPAR subunits, auxiliary subunits, PTMs, trafficking, and synaptic plasticity.
- Main analysis is conceptual: it proposes the AMPAR code and a hierarchy of preferential AMPAR recruitment/removal during LTP, LTD, and homeostatic scaling, drawing on cited knock-in, knockout, molecular replacement, electrophysiology, biochemical, proteomic, and behavioral studies.
Limitations
- Stated: AMPAR subunit combinations have not been systematically analyzed throughout the brain, and earlier long-tail vs. short-tail conclusions may be oversimplified because some studies relied on overexpression of GluA1 or GluA2 in young organotypic hippocampal slices, producing biased homomeric receptors.
- Stated: the role of CP-AMPARs in LTP remains controversial and may depend on a narrow developmental window and time of day; several PTM roles remain undetermined, including whether certain GluA1 PTMs play a role in LTP, the role of AMPAR ubiquitination in LTD, and whether GluA2 ubiquitination and phosphorylation interact during scaling-down.
- Evident: as a review and conceptual framework, the AMPAR code is proposed rather than directly tested; the predicted hierarchy of AMPAR variant recruitment/removal awaits systematic experimental validation.
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Claims the paper makes
56 Partly supported · 27 Own interpretation · 25 Supported · 13 No full text of the sources · 11 Sources not found · 9 Supported so far · 3 No basis given · 1 Mixed support · 1 Not checked yet · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“A primary mechanism in the control of synaptic strength during plasticity is an alteration in the number, composition and biophysical properties of AMPA-type glutamate receptors (AMPARs) in the post-synaptic membrane (Huganir and Nicoll, 2013, Malinow and Malenka, 2002).”
§ The AMPA receptor code of synaptic plasticity > Introduction
What the sources say
- Supportedcites Huganir and Nicoll, 2013 source
The Conclusions and Future Directions section says changes in AMPAR number at synaptic spines mediate changes in synaptic strength during LTP and LTD. The AMPAR Phosphorylation and LTP section describes changes in channel conductance, while the conclusions discuss subunit-specific trafficking during plasticity, supporting the claim about biophysical properties and composition. The indexed passages do not provide page numbers. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites Malinow and Malenka, 2002 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In hippocampal CA1 neurons the majority of AMPARs are made up from GluA1/2 and GluA2/3 subunit combinations, with a small contribution of GluA1 homomers (Wenthold et al., 1996).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Subunit combinations
What the sources say
- Supportedcites Wenthold et al., 1996 source
The paper’s opening summary reports two major AMPA receptor complexes in CA1/CA2 pyramidal neurons—GluR1/GluR2 and GluR2/GluR3—and estimates that about 8% are homomeric GluR1. Its findings include CA1 neurons, although the preparation combined CA1 and CA2 rather than measuring CA1 separately. (LLM, conf=0.91)
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In the paper
“These findings show that the involvement of CP-AMPARs in hippocampal LTP may follow a very narrow developmental window of only a few days.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Sanderson et al., 2016 source
The Discussion reports that CP-AMPAR antagonist sensitivity of hippocampal LTP changes between postnatal days 14 and 17, describing the developmental switch as occurring over only about three days. This supports the claim's qualified wording about a narrow developmental window. (LLM, conf=0.94)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“A recent study that used knock-in mutations demonstrated that two key CaMKII phosphorylation sites on TARP γ-8, S277 and S281, are important mediators of hippocampal LTP and learning and memory (Park et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Supportedcites Park et al., 2016 source
The Results sections (page not available in our copy) identify S277 and S281 as major CaMKIIα phosphorylation sites and report that replacing both with alanine in knock-in mice reduced hippocampal LTP. The same mice showed impaired contextual and cued fear memory under mild training conditions, supporting the claim that these sites are important for learning and memory. (LLM, conf=0.94)
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- Supported
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In the paper
“As described above, LTP has been shown to occur in the absence of certain AMPAR subunits (Granger et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Granger et al., 2013 source
The Discussion reports normal LTP when GluA2(Q) replaced GluA1, showing that LTP can occur without the GluA1 subunit. The section ‘LTP requires a reserve pool of AMPARs’ also reports that deleting GluA2 or GluA3, separately or together, had no effect on LTP. (LLM, conf=0.94)
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In the paper
“GluA4 clustering at excitatory synapses, particularly onto parvalbumin-positive interneurons, is mediated by the extracellular neuronal pentraxins which bind to the extracellular amino terminal domain, again highlighting the role of extracellular interactions in AMPAR synaptic recruitment (Pelkey et al., 2015, O'Brien et al., 1999, Sia et al., 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Pelkey et al., 2015 source
The Results and Discussion describe neuronal pentraxins as AMPAR-clustering proteins and state that they directly associate with GluA4’s N-terminal domain. The same section reports deficient synaptic GluA4 at excitatory synapses onto parvalbumin-positive interneurons when NPTX2 and NPTXR are absent. Page numbers are not available in our copy. (LLM, conf=0.91)
- Not matchedcites O'Brien et al., 1999
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Sia et al., 2007 source
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In the paper
“A recent proteomics study has even found that GluA3 subunits are the most enriched within the PSD under basal conditions (Pandya et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Pandya et al., 2017 sourceExperimental — accuracy not yet measured
In Results and Discussion, “Glutamate receptors and their interacting proteins” (page unavailable), GRIA3/GluA3 shows strong PSD association, but GRIA4 has the same reported 0.99 correlation. The paper therefore supports GluA3 as highly PSD-enriched, not as uniquely the most enriched subunit; it also does not explicitly characterize the comparison as being under basal conditions. (LLM, conf=0.86)
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- Partly supported
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In the paper
“Hippocampal LTP in very young neurons may preferentially recruit CP-AMPARs (Plant et al., 2006, Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Plant et al., 2006 source
- Supportedcites Sanderson et al., 2016 source
In the Results section (“LTP expression is inhibited by antagonism of CP-AMPARs in 2 but not 3 week-old WT mice”; page unavailable), CP-AMPAR antagonism suppressed hippocampal CA1 LTP in P11–14 mice but not P17–21 mice. The Discussion describes this as a developmental switch away from CP-AMPAR engagement in LTP, supporting the hedged claim about very young neurons. (LLM, conf=0.91)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“In cerebellar Purkinje neurons, phosphorylation of GluA2 Y876 has been shown to inhibit subsequent phosphorylation of GluA2 S880 (Figure 1) (Kohda et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Kohda et al., 2013 source
In “Increased Y876 Phosphorylation Inhibited Activity-Induced S880,” prior Src treatment reduced subsequent PKC-mediated S880 phosphorylation in vitro, while a nonphosphorylatable Y876 mutant did not show that effect (Fig. 2C–D). The same section reports that reducing Y876 phosphorylation restored activity-induced S880 phosphorylation in GluD2-null cerebellar slices (Fig. 2E), supporting the claim in the Purkinje-cell context. (LLM, conf=0.92)
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In the paper
“Dephosphorylation of GluA2 Y876 by tyrosine phosphatase PTPMEG was necessary for S880 phosphorylation and expression of cerebellar LTD (Kohda et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Kohda et al., 2013 source
The Discussion states that Y876 phosphorylation prevents subsequent S880 phosphorylation, that Y876 dephosphorylation restores LTD, and that PTPMEG directly dephosphorylates GluA2 Y876. It also reports that GluD2–PTPMEG association was necessary for LTD induction in Purkinje cells. (LLM, conf=0.92)
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In the paper
“Several studies have demonstrated that GluA2 is required for the expression of cerebellar LTD.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Chung et al., 2000 sourceExperimental — accuracy not yet measured
The Discussion says Purkinje-cell AMPA receptors contain GluR2 (GluA2) and that cerebellar LTD may involve AMPA-receptor endocytosis. It does not establish that GluA2 is required for the expression of cerebellar LTD; the paper’s GluR2 experiments concern receptor phosphorylation and internalization, not a test of that requirement. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites Steinberg et al., 2006 source
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In the paper
“LTP in the mature hippocampus is mediated by GluA2-containing receptors (Adesnik and Nicoll, 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Adesnik and Nicoll, 2007 sourceExperimental — accuracy not yet measured
The Introduction says synaptic AMPA receptors in CA1 pyramidal cells generally contain GluR2 (GluA2), and the Discussion concludes that CA1 LTP does not involve inserting calcium-permeable receptors. But the Methods describe slices from 2–3-week-old animals, so the experiments do not establish the claim specifically for the mature hippocampus or for hippocampal regions beyond CA1. (LLM, conf=0.88)
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In the paper
“Another parallel mechanism suggests that PICK1 is important during the early phase of LTP where it acts to sequester GluA2-containing receptors within endosomes, enabling CP-AMPARs to be transiently incorporated into synapses (Jaafari et al., 2012, Clem et al., 2010).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Jaafari et al., 2012 source
The Role of PICK1 section (Fig. 8; pp. 11618–11630) proposes that PICK1 retains GluA2-containing receptors in endosomes immediately after LTP induction while GluA2-lacking, calcium-permeable receptors transiently reach synapses. The paper presents this as a model supported by its glycine-stimulation experiments, consistent with the citing sentence’s hedged wording. (LLM, conf=0.94)
- Not matchedcites Clem et al., 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Our proposed hierarchy suggests that in the absence of preferred AMPAR variants, less preferred variants, or even kainate receptors, may substitute, although this is may be only the case for the most robust LTP induction protocols (Granger et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Granger et al., 2013 sourceExperimental — accuracy not yet measured
The Introduction and the section “GluK1 is sufficient for mediating LTP” report normal LTP after AMPARs were replaced with GluA2 or kainate receptors. The Methods specify the induction protocol, but the paper does not compare protocols or suggest that substitution works only with the most robust ones. The proposed hierarchy is the citing authors’ framing, not a finding attributed to this source. (LLM, conf=0.83)
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In the paper
“To summarize, LTP requires an enhancement of synaptic AMPARs (Huganir and Nicoll, 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
The Long-Term Potentiation section describes LTP-associated increases in AMPAR responses, supporting AMPAR enhancement as a common expression mechanism. But the Subunit Dependence section says LTP can be expressed with exogenously supplied kainate receptors, and the Conclusions say LTP mechanisms can act on either receptor type. Thus, the source does not support an absolute requirement for enhanced synaptic AMPARs. Page numbers were not provided in our copy. (LLM, conf=0.87)
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In the paper
“The GluA2 S880 phosphorylation site has also been shown to be important in hippocampal LTD (Seidenman et al., 2003, Chung et al., 2000, Steinberg et al., 2006).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Seidenman et al., 2003 source
The Introduction reports that preventing GluR2 S880 phosphorylation reduces LTD in hippocampal slice cultures. The Results section likewise reports significantly impaired LTD in cells expressing a phosphorylation-preventing mutant. The paper notes that LTD was reduced, not completely blocked. (LLM, conf=0.94)
- Partly supportedcites Chung et al., 2000 sourceExperimental — accuracy not yet measured
The Discussion links hippocampal LTD to PKC activation and suggests that GluR2 Ser880 phosphorylation may regulate AMPA-receptor internalization during synaptic plasticity. It does not show that the site is important for hippocampal LTD; that specific role remains a proposed connection in this paper. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Steinberg et al., 2006 source
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In the paper
“AMPAR association with the PSD is reduced during scaling-down by increasing the rate at which AMPARs dissociate from the PSD scaffold (Tatavarty et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Supportedcites Tatavarty et al., 2013 source
The Introduction reports that scaling down doubled the rate at which bound AMPARs exited the synapse (Koff) and concludes that AMPARs unbind from synaptic scaffolds faster. The Discussion says this increase in Koff reduces the transiently bound fraction and its occupancy of postsynaptic binding sites. (LLM, conf=0.94)
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In the paper
“indicating that the induction of LTD requires PKA phosphorylation of GluA1 even though receptors are eventually dephosphorylated (Huganir and Nicoll, 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
The “AMPAR Phosphorylation and LTP” section reports significant deficits in LTD induction when GluA1 CaMKII and PKA phosphorylation sites cannot be phosphorylated, and reports that LTD decreases phosphorylation. But it does not establish that PKA phosphorylation of GluA1 is strictly required: the “NMDAR-Dependent LTD” section also notes normal LTD in mice lacking GluA1. (LLM, conf=0.86)
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In the paper
“Dephosphorylation of these two sites enhances the interaction of GluA2 with GRIP1/2 scaffold proteins (Hayashi and Huganir, 2004, Chung et al., 2000).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Not matchedcites Hayashi and Huganir, 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Chung et al., 2000 sourceExperimental — accuracy not yet measured
In “Phosphorylation of GluR2 PDZ ligand differentially regulates its interaction with GRIP1 and PICK1” (page unavailable), dephosphorylating the Ser880-phosphorylated GluR2 peptide restored GRIP1 binding. The passages do not establish that dephosphorylation of Y876 enhances binding or that the effect applies to GRIP2. (LLM, conf=0.88)
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In the paper
“AKAP5 anchors both PKA and CaN to GluA1 allowing for the efficient coordination of these signaling pathways during LTD (Sanderson and Dell'Acqua, 2011).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Sanderson and Dell'Acqua, 2011 source
The Scaffolding proteins section says AKAP79/150 anchors CaN near its PKA anchoring site and links to AMPARs through MAGUK proteins. The AKAP79/150 involvement in LTP and LTD section describes how anchored CaN and PKA coordinate GluR1 (GluA1) dephosphorylation, endocytosis, and rephosphorylation during LTD. The linkage to GluA1 is indirect, rather than direct anchoring to the receptor. (LLM, conf=0.91)
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In the paper
“In response to chronic hyperactivity or hypoactivity, neurons can engage homeostatic scaling-down or scaling-up respectively, in which the strength of excitatory synapses on a neuron is globally modified to maintain neuronal activity in a physiological range (O'Brien et al., 1998, Turrigiano et al., 1998, Turrigiano, 2008).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Not matchedcites O'Brien et al., 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Turrigiano et al., 1998 source
- Supportedcites Turrigiano, 2008 source
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“To summarize, LTD requires a net removal of AMPARs from the post synaptic membrane.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Huganir and Nicoll, 2013 source
The NMDAR-Dependent LTD section says there is a general consensus that reduced synaptic transmission during LTD is due to a loss of synaptic AMPARs. The Dynamic Regulation of AMPAR Membrane Trafficking section also reports rapid AMPAR endocytosis following a treatment used to induce LTD chemically. Together, these support the claim’s summary of net AMPAR removal from the postsynaptic synapse. (LLM, conf=0.86)
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In the paper
“It has been recently shown that this population of peri-synaptic CP-AMPARs (GluA1 homomers) are transiently recruited to the synapse during the induction of LTD in a PKA-dependent manner (Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Sanderson et al., 2016 sourceExperimental — accuracy not yet measured
The Introduction and Results state that GluA1 CP-AMPARs are transiently recruited during LTD induction through AKAP150-anchored PKA signaling. However, the Discussion says the experiments cannot distinguish physical recruitment into the synapse from functional engagement of receptors already at peri-synaptic locations. The claim presents physical recruitment of a peri-synaptic population as settled; page numbers were not supplied in our copy. (LLM, conf=0.85)
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In the paper
“Like in cultured neurons, visual deprivation-induced scaling-up is absent in GluA1 S845A knock-in mutant mice (Goel et al., 2011).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Goel et al., 2011 source
The Results section, “Visual deprivation-induced homeostatic synaptic plasticity is absent in GluR1-S845A mutants,” reports that two days of dark exposure did not change average mEPSC amplitude in the mutants. Figure 3 likewise describes no significant amplitude change, supporting the claim that visual deprivation-induced scaling-up is absent. (LLM, conf=0.94)
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In the paper
“AKAP5 (also called AKAP79/AKAP150) is a signaling scaffold protein required for LTD (Sanderson et al., 2016, Jurado et al., 2010).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Sanderson et al., 2016 source
The Introduction identifies AKAP79/150 as AKAP5 and describes it as a scaffold for PKA and calcineurin. The Results report impaired NMDAR-dependent LTD when AKAP150 anchoring is disrupted, supporting its required role in the LTD mechanism studied. (LLM, conf=0.90)
- Partly supportedcites Jurado et al., 2010 sourceExperimental — accuracy not yet measured
The Abstract identifies AKAP79/150 as a protein scaffold and reports that it is required for NMDA receptor-dependent LTD. The unqualified claim is broader than the finding: the paper reports no detectable effect of AKAP knockdown on mGluR-dependent LTD. (LLM, conf=0.86)
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In the paper
“Consistent with these data, deletion of the GRIP1/2 genes completely blocks scaling-up (Tan et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Tan et al., 2015 source
The “Inactivity-Induced Synaptic Scaling Is Blocked in GRIP Knockout” section reports that TTX-induced inactivity did not increase surface GluA1, GluA2, or GluA3 in GRIP1/2 double-knockout neurons. The paper concludes that loss of GRIP function blocks TTX-induced synaptic scaling up in the cultured neurons studied. (LLM, conf=0.91)
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In the paper
“The majority of these GluA1-containing receptors are likely to be GluA1/2 heteromers (Wenthold et al., 1996, Lu et al., 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Supportedcites Wenthold et al., 1996 source
In the immunoprecipitation section (page unavailable), the paper concludes that most complexes containing GluR1 and another subunit comprise GluR1 and GluR2, while only a small population contains both GluR1 and GluR3. It also estimates that 15–20% of GluR1 is present without GluR2, GluR3, or GluR4. Together, these findings support the qualified claim for the CA1/CA2 preparation studied. (LLM, conf=0.92)
- Not matchedcites Lu et al., 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“Surface localized AMPARs are supplied by exocytosis from pools of intracellular receptors contained within endosomes (Lin et al., 2009, Makino and Malinow, 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Partly supportedcites Lin et al., 2009 sourceExperimental — accuracy not yet measured
The Introduction says AMPARs delivered during LTP are thought to originate from recycling endosomes, and the Results and Discussion describe vesicle insertion at the neuronal surface. The source supports the proposed route but does not establish endosomes as the source of surface AMPARs generally; the claim states that origin without the paper’s qualification. (LLM, conf=0.84)
- Partly supportedcites Makino and Malinow, 2009 sourceExperimental — accuracy not yet measured
The Results section (‘Compartmentalized GluR1 exocytosis replenishing a local extrasynaptic AMPAR pool’; page unavailable) says intracellular GluR1 is exocytosed onto the dendritic surface and replenishes an extrasynaptic receptor pool. Our copy does not identify those intracellular pools as endosomes, so that specific part of the claim is unsupported. (LLM, conf=0.86)
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In the paper
“Large packets of GluA1 are inserted into the dendritic shaft from intracellular recycling endosomes, containing an estimated fifty GluA1-containing receptors, in an activity-dependent manner (Lin et al., 2009, Makino and Malinow, 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Partly supportedcites Lin et al., 2009 sourceExperimental — accuracy not yet measured
The Results (Capturing insertion events of GluRs; page unavailable) report GluR1 insertion in dendritic shafts, and activity suppression reduced its frequency. The Introduction says AMPARs are thought to originate from recycling endosomes, but the paper does not establish that the observed GluR1 packets came from them or estimate fifty receptors per packet; it instead describes vesicles as likely containing a limited number of receptors. (LLM, conf=0.88)
- Partly supportedcites Makino and Malinow, 2009 sourceExperimental — accuracy not yet measured
The Results section, “Small contribution of AMPAR exocytosis to synaptic potentiation during LTP” (page unavailable), reports GluR1-containing compartments undergoing exocytosis onto dendrites after LTP induction. The cited paper does not identify those compartments as recycling endosomes or estimate that each contains fifty receptors; its reported fluorescent spots do not establish the claimed packet size. (LLM, conf=0.87)
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In the paper
“A prominent model of synaptic strength posits that the post-synaptic density (PSD), a dense network of synaptic scaffolding, adhesion and cytoskeletal proteins, contains ‘slots’ that might be occupied by AMPARs supplied by lateral diffusion from the peri-synaptic region (Opazo et al., 2012, Huganir and Nicoll, 2013, Kessels and Malinow, 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Not checked — no full text of the sourcecites Opazo et al., 2012 source
- Supportedcites Huganir and Nicoll, 2013 source
In “Proposed Working Models for LTP,” the paper describes a PSD-centric model in which slots capture mobile AMPARs at the synapse. “Dynamic Regulation of AMPAR Membrane Trafficking” says extrasynaptic AMPARs move laterally into synapses, supporting the proposed route from the surrounding membrane. (LLM, conf=0.92)
- Partly supportedcites Kessels and Malinow, 2009 sourceExperimental — accuracy not yet measured
In “Synaptic Strengthening by AMPAR Trafficking” (page unavailable), the paper describes a synaptic AMPAR ‘slot’ formed by interacting proteins. “Synaptic Trafficking in the Absence of Plasticity” describes receptor exchange from extrasynaptic to synaptic sites. Neither passage specifies lateral diffusion from the perisynaptic region into PSD slots, so that mechanism is not supported by this source. (LLM, conf=0.84)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Decreased phosphorylation of S845 during scaling-down is not mediated by phosphatase activation, but rather by a decrease in PKA targeting to the synapse through uncoupling with the AKAP5 scaffold, favoring the dephosphorylated state of GluA1 (Figure 3) (Diering et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Supportedcites Diering et al., 2014 source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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In the paper
“The AMPAR code predicts that under certain conditions the PSD slots will have biased affinity towards certain AMPAR variants, for example phosphorylated GluA1-containing receptors during noradrenaline facilitated hippocampal LTP (Makino et al., 2011, Hu et al., 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Partly supportedcites Makino et al., 2011 sourceExperimental — accuracy not yet measured
In the Discussion model, Makino et al. propose that GluA1 phosphorylation may increase interactions with scaffolding proteins in a perisynaptic microdomain, making the receptors easier to insert into synapses. The Results also show that norepinephrine phosphorylates GluA1 in hippocampal slices and permits LTP after weak stimulation. The paper does not establish that PSD slots have biased affinity for phosphorylated GluA1-containing receptors; its proposed scaffolding mechanism is qualified and perisynaptic. (LLM, conf=0.84)
- Not matchedcites Hu et al., 2007
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plainconditional- Asserted: passes — The authors put it forward as true.
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- Partly supported
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In the paper
“It has been shown that phosphorylated GluA1 S845 is resistant to ubiquitination (Guntupalli et al., 2017), offering a potential mechanism for the differential removal of phosphorylated and unphosphorylated GluA1 during scaling-down.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Supportedcites Guntupalli et al., 2017 source
In Results, under “The cross-talk between GluA1 phosphorylation and ubiquitination” (page not provided), the S845D phosphomimetic showed reduced AMPA-induced GluA1 ubiquitination relative to wild type. The authors conclude that Ser-845 phosphorylation negatively regulates ubiquitination. The experiment supports “resistant” as reduced susceptibility, not complete immunity. (LLM, conf=0.91)
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The AMPAR code suggests that AMPAR variants will be predictive of the types and extent of synaptic plasticity which can occur”
§ The AMPA receptor code of synaptic plasticity > Abstract
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In the paper
“This code suggests that AMPAR subunit combinations, assembly in larger protein complexes, and PTMs may be a mode of information storage involved in synaptic computation, plasticity and learning and memory.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“The function and the trafficking of AMPARs to and from synapses is modulated by specific AMPAR GluA1-4 subunits, subunit specific protein interactors, auxiliary subunits, and post-translational modifications.”
§ The AMPA receptor code of synaptic plasticity > Abstract
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In the paper
“Moreover, many modifications and interactions have been shown to occur in combinations or to have feedback effects on neighboring modification sites or protein interactions, such that certain combinations of PTMs and interactions may be favored or inhibited.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“The types, thresholds and range of synaptic plasticity available for any synapse is likewise determined by the nature of the AMPARs already at synapses which could be modified or those which can be added to synapses during potentiation or removed during depression.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“a hierarchy exists such that certain AMPARs will be disproportionally recruited to synapses during LTP/homeostatic scaling-up, or removed during LTD/homeostatic scaling-down.”
§ The AMPA receptor code of synaptic plasticity > Abstract
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In the paper
“As the majority of research is done during the light phase, when CP-AMPARs are less prevalent, this finding suggests that some of the controversy regarding CP-AMPARs may also be subject to time of day effects.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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- Rests on an assumption: The majority of research is done during the light phase, when CP-AMPARs are less prevalent.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Each step of synapse targeting is subject to AMPAR subunit composition, auxiliary subunit interaction, and PTMs.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“The ability of the AMPAR core to interact with auxiliary subunits in a mixed stoichiometry, the selective interaction of auxiliary subunits with certain AMPAR subunit combinations, and the role of auxiliary proteins in the effect of AMPAR PTMs substantially increase the functional complexity of the AMPAR code.”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
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In the paper
“Thus, the number and function of AMPARs contained within synapses is dictated by a series of equilibriums and by individual channel properties.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“An emerging theme from these studies suggests that endosomal pools of GluA2 or GluA3, possibly in the form of GluA1-containing heteromeric receptors, are mobilized to the cell-surface to facilitate LTP.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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In the paper
“GluA4 S842 is phosphorylated by PKA (Esteban et al., 2003).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Esteban et al., 2003 source
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In the paper
“The period of early postnatal life when GluA4 is expressed also coincides with a period where PKA, and not CaMKII, is required for hippocampal LTP (Yasuda et al., 2003).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Yasuda et al., 2003 source
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In the paper
“Unlike GluA1 where the activity of PKA and CaMKII are coordinated for synaptic recruitment, PKA phosphorylation of GluA4 alone is sufficient for synapse delivery and retention (Esteban et al., 2003).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Esteban et al., 2003 source
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In the paper
“Spike-timing and noradrenaline-dependent LTP in the cortex, for example, will preferentially recruit phosphorylated S845 GluA1-containing receptors (Seol et al., 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Seol et al., 2007 source
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In the paper
“The AMPAR code proposes that a hierarchy exists for the selective incorporation of AMPAR subunit/PTM combinations, such that each form of LTP will favor the recruitment of specific AMPAR types (Figure 2).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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In the paper
“GluA2 Y876 has been identified as a target for Src family tyrosine kinases (Hayashi and Huganir, 2004).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Hayashi and Huganir, 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“During hippocampal mGluR-LTD, concomitant ligand binding and dephosphorylation of GluA2 Y876 stimulates BRAG2 GEF activity, leading to activation of Arf6 driving GluA2 endocytosis (Scholz et al., 2010).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not checked — no full text of the sourcecites Scholz et al., 2010 source
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In the paper
“These studies support a model where GRIP1/2 bind directly to the PDZ ligand in the GluA2/3 C-terminal tail, anchoring the receptors in the PSD (Anggono and Huganir, 2012).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Anggono and Huganir, 2012
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The threshold and nature of induction as well as the magnitude and stability of LTP is therefore the product of the types of AMPARs which are available for synaptic recruitment.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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In the paper
“We propose that all forms of LTP will show a hierarchy of AMPAR recruitment.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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In the paper
“Zhou et al., have recently reported that knock-in mice in which the GluA2 C-tail is replaced with the GluA1 C-tail: GluA2C1KI, are completely impaired in hippocampal NMDAR-dependent LTD (Zhou et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“Similar to LTP and LTD, synaptic strength is altered during homeostatic scaling by changing the abundance of post-synaptic AMPARs (O'Brien et al., 1998).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Not matchedcites O'Brien et al., 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the context of the AMPAR code, we propose that at synapses that contain mixed AMPAR subunits and PTMs, a hierarchy exists such that certain AMPAR variants will be disproportionally targeted for removal during LTD, for example, GluA2/3 containing receptors phosphorylated at S880 (Figure 2).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
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In the paper
“Interestingly, in this study, mGluR-dependent LTD was not affected by the GluA1/2 C-tail exchange.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As both homeostatic and Hebbian forms of synaptic plasticity involve the trafficking and modification of AMPARs it is completely impossible for the different plasticity types to occur independently.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
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In the paper
“Block of endocytosis has been shown in many studies to prevent LTD, suggesting that AMPARs must be locally depleted from the cell surface, perhaps to prevent rapid refilling of the PSD-slots.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Not matchedcites many studies
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The studies on the role of AMPAR phosphorylation during homeostatic scaling suggest that removal of AMPARs from synapses during scaling-down may follow a hierarchy whereby dephosphorylated receptors are preferentially removed.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This recruitment or removal follows a hierarchy, with biased trafficking, accumulation or removal of certain AMPAR variants (Figure 2).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
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In the paper
“We propose that through subunit specific PTMs and protein interactions, layers of regulation are built into the AMPARs such that each form of synaptic plasticity will result in the recruitment or removal of the correct types and number of AMPARs from PSD slots (Zhou et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As new PSD slots are formed during LTP, or as existing slots increase their affinity for AMPARs, the large and localized activity-dependent increase in extra-synaptic GluA1 favors the accumulation of GluA1 at potentiated synapses.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 81
- Probably not a substantial claim. 2
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“CNIH and TARPs likely compete for the same AMPAR binding sites (Straub and Tomita, 2012, Herring et al., 2013), and so one possible function of CNIH is to regulate the stoichiometry of TARP interaction, tuning the channel properties of the associated AMPARs.”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Supportedcites Straub and Tomita, 2012 source
In “Roles of CNIH2/3 in regulating AMPA receptors in the brain” (page unavailable), the review says CNIH2 and TARPs interact competitively with AMPARs and that CNIH2/3 may displace TARPs to control TARP stoichiometry. The same section links TARP stoichiometry to channel properties, supporting the citing sentence’s hedged interpretation. (LLM, conf=0.88)
- Disputedcites Herring et al., 2013 sourceExperimental — accuracy not yet measured
The Results section (‘TARP γ-8 reverses…’; page unavailable) says that unchanged γ-8/AMPAR stoichiometry strongly argues CNIH-2 does not displace γ-8 and that the two can co-occupy GluA1 subunits. The Discussion (‘A model for the interaction…’; page unavailable) proposes four γ-8 molecules on the receptor combinations examined, contrary to CNIH regulating TARP stoichiometry by competing for those sites. The paper does report a different, subunit-specific interaction: γ-8 prevents CNIH from interacting with non-GluA1 subunits. (LLM, conf=0.89)
Checked by a reasoning model — may be wrong.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“AMPARs are highly dynamic, undergoing continuous endocytosis, exocytosis, lateral diffusion in the plane of the membrane, reversible trapping at synapses at the post-synaptic density (PSD), and modifications in channel properties (Opazo et al., 2012, Huganir and Nicoll, 2013, Malinow and Malenka, 2002).”
§ The AMPA receptor code of synaptic plasticity > Introduction
What the sources say
- Not checked — no full text of the sourcecites Opazo et al., 2012 source
- Supportedcites Huganir and Nicoll, 2013 source
The Dynamic Regulation of AMPAR Membrane Trafficking section (page not supplied) describes rapid endocytosis, recycling to the membrane, lateral diffusion, and reduced mobility at synapses. Proposed Working Models for LTP says AMPARs enter and exit the PSD, while AMPAR Phosphorylation and LTP reports changes in channel conductance. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites Malinow and Malenka, 2002 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Interestingly, ubiquination and phosphorylation of GluA1 reciprocally inhibit each other indicating that a complex cross talk of GluA1 PTMs may regulate LTP expression (Guntupalli et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Guntupalli et al., 2017 sourceExperimental — accuracy not yet measured
The Results section, “The cross-talk between GluA1 phosphorylation and ubiquitination” (page unavailable), supports reciprocal inhibition at GluA1 Ser-845: ubiquitin-deficient mutants showed increased phosphorylation, while an S845D phosphomimetic showed reduced ubiquitination. The paper links this cross-talk to AMPA receptor trafficking and surface expression, but does not establish that it regulates LTP expression. (LLM, conf=0.85)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“During hippocampal LTP, PKC is activated to increase GluA1 S818 phosphorylation and a peptide mimicking phospho-GluA1 S818 or shRNA-mediated knock-down of 4.1N both lead to decay of hippocampal LTP back to baseline, suggesting that the PKC/4.1N mediated increase in GluA1 exocytosis is necessary to maintain LTP (Lin et al., 2009, Boehm et al., 2006).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Lin et al., 2009 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites Boehm et al., 2006 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“AMPARs are substrates for cAMP-dependent kinase (PKA) and cGMP-dependent kinase (PKG) (GluA1 S845; GluA4 S842), protein kinase C (PKC) (GluA1 S818/S831/T840; GluA2 S863/S880), Ca++/calmodulin dependent kinase II (CaMKII) (GluA1 S567/S831), Casein kinase II (GluA1 S579; GluA2 S588), PAK3 (GluA1 S863), and Src family tyrosine kinase (GluA2 Y876) (Roche et al., 1996, Barria et al., 1997a, Barria et”
§ The AMPA receptor code of synaptic plasticity > Introduction > Post-translational modifications of AMPAR subunits
What the sources say
- Partly supportedcites Roche et al., 1996 sourceExperimental — accuracy not yet measured
The Phosphorylation of Ser-845 and Ser-831 sections support PKA phosphorylation of GluR1 (GluA1) S845 and PKC phosphorylation of GluR1 S831. The cited paper also discusses CaMKII phosphorylation of GluR1 generally, but our copy does not establish the sentence’s other specified kinase–site pairings, including PKG, casein kinase II, PAK3, and Src pairings. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Not matchedcites Barria et al., 1997a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Barria et al., 1997b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These receptors have faster decay kinetics but large conductance, enhancing synaptic transmission, and may activate unique Ca2+-sensitive signaling pathways which lead to an opening of a metaplastic state, in which synapses become primed for LTD or LTP (Clem and Huganir, 2010, Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Subunit combinations
What the sources say
- Not matchedcites Clem and Huganir, 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Sanderson et al., 2016 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“GluA1 directly interacts with the cytoskeletal scaffold protein 4.1N through the C-terminal juxtamembrane region, and this interaction promotes activity-dependent exocytosis of GluA1 from intracellular endosomes (Lin et al., 2009, Anggono and Huganir, 2012).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Lin et al., 2009 sourceExperimental — accuracy not yet measured
The Introduction and Results describe 4.1N binding to the membrane-proximal region of GluR1 (GluA1) and its role in activity-dependent insertion at the extrasynaptic surface. The Introduction says AMPARs are *thought* to originate from recycling endosomes, but the paper does not establish that the 4.1N-dependent GluR1 insertion events specifically come from intracellular endosomes. (LLM, conf=0.84)
- Supportedcites Anggono and Huganir, 2012 source
The Protein 4.1N section (page unavailable) says 4.1N binds directly to the membrane-proximal region of the GluA1 C-terminal domain and that its knockdown reduces GluA1 insertion into the plasma membrane. The AMPA Receptor Trafficking and AMPA Receptor Interacting Proteins sections (pages unavailable) describe delivery from AMPAR-containing vesicles or endosomes and GluA1’s role in activity-dependent exocytosis. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These findings, together with several previous studies, support a model where PKA-mediated phosphorylation of GluA1 S845 promotes the surface trafficking of the receptor, lowering the threshold needed to induce LTP, however, additional signaling from CaMKII is needed to promote GluA1 targeting to the PSD for maximal LTP (Figure 1) (Sun et al., 2005, Oh et al., 2006, Esteban et al., 2003).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Sun et al., 2005 sourceExperimental — accuracy not yet measured
The Discussion reports that D1–PKA signaling increases extrasynaptic GluR1 surface expression and that CaMKII is also needed for synaptic delivery. The section on D1 receptor stimulation shows that pretreatment enables a normally subthreshold glycine concentration to increase synaptic GluR1 incorporation. Our copy does not establish phosphorylation specifically at S845, directly measure a lowered LTP-induction threshold, or address maximal LTP or PSD targeting. (LLM, conf=0.88)
- Not matchedcites Oh et al., 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Esteban et al., 2003 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“NMDAR-dependent LTP requires Ca2+ influx leading to activation of CaMKII/PKC which directly phosphorylate GluA1 S831, increasing GluA1 single channel conductance and promoting GluA1 targeting to the PSD (Mammen et al., 1997, Barria et al., 1997a, Derkach et al., 1999, Kristensen et al., 2011, Barria et al., 1997b).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not checked — no full text of the sourcecites Mammen et al., 1997 source
- Not matchedcites Barria et al., 1997a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Derkach et al., 1999 sourceExperimental — accuracy not yet measured
The Abstract and Results report that CaMKII phosphorylation of GluR1 (GluA1) at Ser-831 increases the contribution of higher single-channel conductance states. The paper also says PKC phosphorylates Ser-831, but treats its effect on conductance as presumptive. It does not establish NMDAR dependence or show that this phosphorylation promotes GluA1 targeting to the postsynaptic density. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The major form of LTP identified in the brain, NMDAR-dependent LTP, is the result of increased AMPAR density in the post-synaptic membrane and/or single channel conductance of the AMPAR (Huganir and Nicoll, 2013, Herring and Nicoll, 2016, Poncer et al., 2002, Benke et al., 1998).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Huganir and Nicoll, 2013 source
The Dynamic Regulation of AMPAR Membrane Trafficking section reports that AMPARs are recruited to synaptic spines after LTP induction, alongside synaptic strengthening. The AMPAR Phosphorylation and LTP section reports changes in AMPAR single-channel conductance after LTP and describes how phosphorylation regulates that conductance. Together, these passages support the stated postsynaptic mechanisms. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Herring and Nicoll, 2016 source
- Partly supportedcites Poncer et al., 2002 sourceExperimental — accuracy not yet measured
The introductory passage and Discussion describe increased synaptic AMPAR number and channel conductance as mechanisms associated with LTP in CA1 hippocampal neurons. The paper does not establish that these mechanisms explain NMDAR-dependent LTP throughout the brain; its own experiments test whether activated CaMKII mimics LTP-related effects in CA1 neurons. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TARPs have been shown to stabilize AMPARs both on the cell surface and at synapses (Bats et al., 2007, Sheng et al., 2018), and loss of TARPs results in decreased AMPAR expression, suggesting that “TARPless” AMPARs become unstable (Fukaya et al., 2006, Chen et al., 2000).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Not checked — no full text of the sourcecites Bats et al., 2007 source
- Partly supportedcites Sheng et al., 2018 sourceExperimental — accuracy not yet measured
The Discussion reports that the PDZ ligand of TARP γ-8 is essential for moving surface AMPARs to synapses, supporting the synaptic part of the claim. The Results report equal surface AMPAR currents with intact γ-8 and a PDZ-motif-deficient mutant; the paper does not establish that TARPs stabilize AMPARs on the cell surface. The decreased-expression and instability clause is attributed to other citations, not Sheng et al. (LLM, conf=0.86)
- Partly supportedcites Fukaya et al., 2006 sourceExperimental — accuracy not yet measured
The Results section (‘Selective reduction of hippocampal AMPA receptors in γ-8-KO mice’; page unavailable) reports substantially lower hippocampal AMPA receptor levels after γ-8 deletion. The Discussion (‘Differences between the present and preceding studies’; page unavailable) suggests that receptors redistributed toward cell bodies are presumably degraded. The study does not establish that those receptors lack all TARPs or directly show that TARP-free receptors are unstable. (LLM, conf=0.84)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TARPs and CNIH2/3 regulate AMPAR channel properties and cellular and synaptic trafficking (Straub and Tomita, 2012, Maher et al., 2017, Jacobi and von Engelhardt, 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Partly supportedcites Straub and Tomita, 2012 sourceExperimental — accuracy not yet measured
The Conclusions state that TARPs modulate both AMPAR trafficking and channel properties, while CNIH2/3 modulate AMPAR channel properties. The section “Roles of CNIH2/3 in regulating AMPA receptors in the brain” reports enhanced AMPAR surface expression in heterologous cells but says whether CNIH2/3 promote trafficking in hippocampal neurons remains unresolved. Thus the claim overstates CNIH2/3’s established role in synaptic trafficking. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Maher et al., 2017 source
- Not checked — no full text of the sourcecites Jacobi and von Engelhardt, 2017 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This method would dramatically disrupt the composition of synapses and may not reflect the physiological mechanisms underlying LTP expression (Sheng et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Sheng et al., 2013 source
In “One step forward,” the paper says Granger et al. deleted the genes encoding three AMPA-receptor subunits, leaving endogenous AMPA receptors absent. In “Two steps back,” it cautions that this deletion may fundamentally change receptor trafficking compared with normal synapses and recommends subtler manipulations to study LTP mechanisms at normal synapses. Page numbers are not provided in our copy. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Phosphorylation of S845 increases single channel open–probability and also promotes GluA1 targeting or retention to the cell surface (Banke et al., 2000, Oh et al., 2006, Man et al., 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Banke et al., 2000 sourceExperimental — accuracy not yet measured
The Discussion states that phosphorylation of GluR1 Ser845 by PKA appears to increase peak open probability, supporting the first part of the sentence. The passages on recombinant receptor function and the additional search do not establish that Ser845 phosphorylation promotes targeting or retention at the cell surface. (LLM, conf=0.88)
- Not matchedcites Oh et al., 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Man et al., 2007 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TARP γ-8 effectively prevented CNIH2/3 interaction with GluA2/3 heteromeric receptors suggesting that CNIH proteins may control the subunit composition of synaptic AMPARs (Herring et al., 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Partly supportedcites Herring et al., 2013 sourceExperimental — accuracy not yet measured
The Discussion’s model for GluA2A3 heteromers says the receptors did not coimmunoprecipitate CNIH-2 and proposes that they contain γ-8 but no CNIH, supporting the proposed link to synaptic AMPAR subunit composition. It calls γ-8’s inhibition of CNIH interaction with GluA3 speculative, however, so the claim presents that mechanism more definitively than the paper does. Page numbers were not available in our copy. (LLM, conf=0.82)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The presence of perisynaptic CP-AMPARs as well as their recruitment to synapses requires signaling from PKA and the S845 phosphorylation site (He et al., 2009, Clem and Huganir, 2010, Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not matchedcites He et al., 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Clem and Huganir, 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Sanderson et al., 2016 sourceExperimental — accuracy not yet measured
The Introduction reports PKA-dependent recruitment of CP-AMPARs to synapses during LTD induction, and the Discussion says a perisynaptic CP-AMPAR pool was absent in S845A mice (page numbers unavailable). The paper does not establish that PKA signaling is required for the presence of that perisynaptic pool; it also acknowledges uncertainty about whether recruitment is physical or functional. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“S-nitrosylation of GluA1 C875 by nNOS was found to enhance the phosphorylation of GluA1 S831 by CaMKII (Figure 1) (Selvakumar et al., 2013), suggesting an additional synergistic relationship between S831 phosphorylation and C875 nitrosylation.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Selvakumar et al., 2013 sourceExperimental — accuracy not yet measured
The Results and Discussion report that nNOS-derived NO nitrosylates GluA1 at C875 and facilitates S831 phosphorylation. However, the direct phosphorylation experiments described in the Results used PKC stimulation; the CaMKII experiments measured changes in channel conductance, not a direct enhancement of CaMKII-mediated S831 phosphorylation by C875 nitrosylation. Page numbers were not available in our copy. (LLM, conf=0.85)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“All four AMPAR subunit are also ubiquitinated. The major sites of ubiquitination on GluA1 and GluA2 have been mapped to GluA1 K868 and GluA2 K870/K882 (Widagdo et al., 2015, Widagdo et al., 2017, Lussier et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Post-translational modifications of AMPAR subunits
What the sources say
- Supportedcites Widagdo et al., 2015 source
The Results section, “All Four AMPAR Subunits Are Ubiquitinated in an Activity- and Ca2+-Dependent Manner,” reports ubiquitination of GluA1–4 after AMPA or bicuculline treatment. The Results section, “GluA1 and GluA2 Are Ubiquitinated on C-Terminal Lysine Residues,” identifies GluA1 Lys-868 and GluA2 Lys-870/Lys-882 as the major sites. (LLM, conf=0.95)
- Supportedcites Widagdo et al., 2017 source
The section “Ubiquitination of AMPARs Is Ca2+-Dependent” states that all four subunits, GluA1–4, undergo activity-dependent ubiquitination. It also identifies Lys-868 as the major GluA1 site and Lys-870 and Lys-882 as the predominant GluA2 sites in neurons. (LLM, conf=0.95)
- Partly supportedcites Lussier et al., 2015 sourceExperimental — accuracy not yet measured
The Ubiquitination section (page not provided) reports that proteomic studies identified all four AMPAR subunits, GluA1–4, as ubiquitinated. Our copy does not identify GluA1 K868 or GluA2 K870/K882 as major ubiquitination sites; searches for those residues found no supporting passage. (LLM, conf=0.87)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Phosphorylation reduces the interaction with membrane lipids and facilitates interaction with PSD95, serving to trap the TARP/AMPAR complex with the PSD (Opazo et al., 2012, Bats et al., 2007, Sheng et al., 2018).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Auxiliary subunits
What the sources say
- Not checked — no full text of the sourcecites Opazo et al., 2012 source
- Not checked — no full text of the sourcecites Bats et al., 2007 source
- Partly supportedcites Sheng et al., 2018 sourceExperimental — accuracy not yet measured
The Discussion (page not available) proposes that PSD-95 can capture AMPAR/TARP complexes through their PDZ ligands, supporting the trapping portion of the claim. It does not say that phosphorylation of the TARP C-terminus reduces membrane-lipid binding or facilitates PSD-95 binding; the phosphorylation described in that model is of synGAP. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Several major forms of LTD described in the brain including, cerebellar LTD and NMDAR-dependent and mGluR-dependent LTD, are expressed by a decrease in synaptic AMPAR content (Huganir and Nicoll, 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
The NMDAR-Dependent LTD section says there is general consensus that LTD-related depression reflects a loss of synaptic AMPARs. The Cerebellar LTD section describes AMPAR endocytosis and retention of GluA2 inside the cell. Although it says mGluR1 activation induces cerebellar LTD, the passages do not establish the claim for mGluR-dependent LTD as a separately named form. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recently, it has been found that LTP in cerebellar Purkinje neurons as well as cerebellar-dependent adaptation of the vestibulo-ocular reflex both depend on GluA3- but not GluA1-containing AMPARs (Gutierrez-Castellanos et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Gutierrez-Castellanos et al., 2017 source
The Introduction states that adaptation of compensatory eye movements depends on GluA3-containing, but not GluA1-containing, AMPARs, and that GluA3-containing AMPARs are critical for parallel-fiber–Purkinje-cell LTP. The Results section reports vestibulo-ocular learning deficits in GluA3-knockout mice but not GluA1-knockout mice. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Via its BAR-domain, PICK1 can either promote the invagination of the plasma membrane or direct GluA2 to regions of invagination where clathrin-mediated endocytosis occurs (Xia et al., 2000, Fiuza et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not checked — no full text of the sourcecites Xia et al., 2000 source
- Partly supportedcites Fiuza et al., 2017 sourceExperimental — accuracy not yet measured
The Introduction and Discussion (‘AMPAR clustering at CCPs’; page not provided) support PICK1-dependent targeting of GluA2-containing receptors to clathrin-coated endocytic sites, with AP2 binding at or adjacent to PICK1’s BAR domain. They do not establish that PICK1’s BAR domain itself promotes plasma-membrane invagination; the paper instead describes its interaction with dynamin and stimulation of dynamin polymerization. (LLM, conf=0.86)
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In the paper
“Here it was shown GluA3 containing receptors are mostly inert under basal conditions due to a very low-open probability, although these receptors are robustly targeted to synapses (Renner et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Renner et al., 2017 source
The Results section reports that GluA2/3 receptors have a low open-channel probability under basal conditions and are largely electrically quiet. A separate Results section finds that they are constitutively inserted into synapses, supporting the claim that synaptic targeting occurs despite their low basal activity. (LLM, conf=0.94)
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- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Consistent with this model, genetic deletion of GRIP1/2 or PICK1 eliminates cerebellar LTD (Takamiya et al., 2008, Steinberg et al., 2006).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Takamiya et al., 2008 source
The Results report that deleting both GRIP1 and GRIP2 abolished LTD in cultured mouse Purkinje cells; deleting either one alone did not. The Introduction also reports that mice lacking PICK1 do not express LTD, citing Steinberg et al. (2006) for that finding. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites Steinberg et al., 2006 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
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In the paper
“This form of cerebellar LTP does not appear to involve trafficking of GluA3, but rather relies on an increase in the open-probability of GluA3-containing receptors through a cAMP-dependent pathway (Gutierrez-Castellanos et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Gutierrez-Castellanos et al., 2017 source
The Introduction states that PF–PC LTP depends on GluA3-containing receptors through changes in channel open probability rather than receptor trafficking, and requires cAMP-mediated Epac activation. The Discussion adds that the evidence against trafficking applies at least over tens of minutes, consistent with the citing sentence’s cautious wording. (LLM, conf=0.93)
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- Supported
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In the paper
“Multiple studies have shown both in slice physiology experiments and in vivo that treatment with a short peptide mimicking the tyrosine-rich region of GluA2 (called the 3Y peptide) completely blocks LTD as well as activity-dependent GluA2 endocytosis (Fox et al., 2007, Ahmadian et al., 2004), while having no effect on basal synaptic transmission.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not checked — no full text of the sourcecites Fox et al., 2007 source
- Partly supportedcites Ahmadian et al., 2004 sourceExperimental — accuracy not yet measured
The hippocampal-slice results (Figure 7) report that GluR2 3Y significantly reduced LFS-induced LTD, while the slice recordings (Figure 6) report no effect on basal synaptic transmission. The cultured-neuron experiments (Figure 8) show blockade of insulin-stimulated AMPA receptor endocytosis, not endocytosis directly measured after activity-induced LTD. This paper therefore does not establish complete blockade of activity-dependent endocytosis or provide in vivo evidence. (LLM, conf=0.88)
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In the paper
“Data show that the amino terminal domain is not necessary for the formation of functional ion channels, or delivery onto the cell surface, but is required for targeting and retention of GluA1 at synapses during LTP (Watson et al., 2017, Diaz-Alonso et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Partly supportedcites Watson et al., 2017 sourceExperimental — accuracy not yet measured
The Results section ('GluA1 requires the NTD for synaptic delivery'; page unavailable) shows that GluA1 lacking its N-terminal domain produces surface currents but fails to incorporate effectively at synapses. The LTP Results and Discussion show that potentiation cannot be maintained without the domain. However, the Discussion also reports transient potentiation and apparent synaptic incorporation of GluA1 lacking the domain, so the claim that it is required for initial targeting during LTP is too strong. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Diaz-Alonso et al., 2017 source
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- Partly supported
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In the paper
“Interestingly, hippocampal mGluR-mediated LTD involves the dephosphorylation of GluA2 Y876 and is completely blocked by inhibitors of tyrosine phosphatases (Moult et al., 2006, Gladding et al., 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Moult et al., 2006 sourceExperimental — accuracy not yet measured
The section on DHPG-LTD and AMPAR dephosphorylation (page unavailable) reports reduced tyrosine phosphorylation of GluR2 in hippocampal slices, but does not identify residue Y876. The section on PTP inhibitors (page unavailable) reports that orthovanadate and phenylarsine oxide prevented significant DHPG-LTD, supporting the inhibitor-blockade portion under the tested conditions. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Gladding et al., 2009 source
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- Partly supported
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In the paper
“Glutamate receptor agonists, including glutamate, AMPA and NMDA, induce GluA2 tyrosine phosphorylation which disrupts the interaction between GluA2 and GRIP1/2 but not PICK1 (Hayashi and Huganir, 2004).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Hayashi and Huganir, 2004 source
The ‘Activation of glutamate receptors’ section reports that glutamate, AMPA, and NMDA each increased GluR2 (GluA2) C-terminal tyrosine phosphorylation in cultured cortical neurons. The ‘Different regulation of GluR2-interacting molecules’ section reports that this phosphorylation impaired binding to GRIP1/2 but did not affect binding to PICK1. Page numbers were not available in our copy. (LLM, conf=0.93)
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In the paper
“Phosphorylation of GluA2 S880 prevents GRIP1/2 binding and promotes the interaction of the GluA2 PDZ ligand with PICK1 (Seidenman et al., 2003, Chung et al., 2000, Steinberg et al., 2006), destabilizing GluA2 within the PSD and promoting GluA2 endocytosis.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Seidenman et al., 2003 source
The Introduction states that S880 phosphorylation disrupts GluR2 binding to GRIP/ABP but not PICK1. The Discussion describes GRIP/ABP as anchoring GluR2 at synapses and proposes that phosphorylation shifts binding toward PICK1, increasing internalization and causing a net loss of synaptic receptors. Page numbers are not provided in the supplied passages. (LLM, conf=0.91)
- Partly supportedcites Chung et al., 2000 sourceExperimental — accuracy not yet measured
The binding-results section shows that Ser880 phosphorylation prevents GluR2 (GluA2) binding to GRIP1 while preserving binding to PICK1; it does not show increased PICK1 binding or test GRIP2. The Discussion and the section on PKC-induced internalization report increased GluR2 internalization alongside Ser880 phosphorylation, but do not establish that phosphorylation itself destabilizes GluR2 within the PSD or causes endocytosis. Page numbers were not available in our copy. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Steinberg et al., 2006 source
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In the paper
“Mice lacking PICK1, KIBRA or Grasp1 all show reductions in hippocampal LTP as well as defects in hippocampus-dependent learning and memory tasks (Makuch et al., 2011, Volk et al., 2010, Chiu et al., 2017)”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Supportedcites Makuch et al., 2011 source
Makuch et al. support the KIBRA portion of the multi-citation claim. The Results report reduced hippocampal LTP in adult KIBRA knockout mice and impaired retention in hippocampus-dependent fear-memory tasks; they note that the plasticity deficit was not seen in juvenile mice. The PICK1 and Grasp1 portions are attributed to the other citations, not judged here. (LLM, conf=0.94)
- Partly supportedcites Volk et al., 2010 sourceExperimental — accuracy not yet measured
The Discussion reports impaired hippocampal LTP with a pairing protocol in adult PICK1-KO mice, while other LTP protocols showed no difference. The Results report impaired inhibitory-avoidance learning in adults, but neither LTP nor learning was impaired in juvenile PICK1-KO mice. The source therefore supports the PICK1 portion of the sentence, but not its unqualified implication that these deficits occur across ages or LTP protocols; the other genes are outside this source's attribution. (LLM, conf=0.87)
- Supportedcites Chiu et al., 2017 source
Chiu et al. support the Grasp1 portion of the multi-citation sentence. In the Results sections on synaptic plasticity and cognitive function (pages not provided), Grasp1 knockout mice show reduced LTP and impaired performance on hippocampus-dependent learning and memory tasks. (LLM, conf=0.94)
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“GluA2 is also a target of ubiquitination on K870 and K882, which occurs in response to neuronal activity and is dependent on AMPAR internalization (Widagdo et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Widagdo et al., 2015 source
The Results section identifies GluA2 K870 and K882 as major sites of AMPA-induced ubiquitination. A separate Results passage reports that blocking endocytosis abolished activity-induced AMPAR ubiquitination, demonstrating that it occurs after internalization. Page numbers are unavailable in our copy. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Specifically, phosphorylation of GluA2 S880 is required as knock-in mutations that prevent phosphorylation of this site in mice (GluA2 K882A) eliminates cerebellar LTD (Chung et al., 2000, Steinberg et al., 2006).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Chung et al., 2000 sourceExperimental — accuracy not yet measured
The ‘PKC phosphorylates serine-880 of GluR2’ section establishes phosphorylation at this site, and the Discussion suggests it may regulate AMPA-receptor internalization during synaptic plasticity. The paper does not establish that S880 phosphorylation is required for cerebellar LTD or report that a K882A knock-in eliminates it. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Steinberg et al., 2006 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Scaling-up can be rescued by expression of shRNA-resistant WT GluA2, but not by a GluA2 chimera with the C-tail swapped for GluA1, suggesting that elements of the GluA2 C-terminus are required for scaling-up (Gainey et al., 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Gainey et al., 2009 source
The Introduction states that shRNA-resistant GluR2 rescues scaling in GluR2-knockdown neurons, whereas a GluR2 chimera bearing the GluR1 C-terminal domain does not. The Results section, “The GluR2 C-Tail is required for the expression of synaptic scaling,” reports the same comparison and concludes that the GluR2 C-tail is essential. (LLM, conf=0.95)
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In the paper
“A phosphorylation site was identified in the first intracellular loop of GluA1 (S567) which is phosphorylated by CaMKII and promotes removal of GluA1 from synapses (Lu et al., 2010, Coultrap et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Lu et al., 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Coultrap et al., 2014 source
The Results section reports CaMKII-dependent phosphorylation of GluA1 at S567 and identifies S567 as a CaMKII substrate site. The Discussion states that S567 phosphorylation decreases synaptic GluA1 localization and describes synaptic GluA1 removal by this phosphorylation. Page numbers are not provided in our copy. (LLM, conf=0.93)
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In the paper
“Scaling-up involves an increase in phosphorylation of GluA1 S845, but not S831, and is completely blocked in neurons with GluA1 S845A knock-in mutations, but remains intact in GluA1 S831A mutant neurons (Diering et al., 2014, Kim and Ziff, 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Diering et al., 2014 source
The Results section, “Changes in AMPAR phosphorylation during homeostatic scaling” (page unavailable), reports that 48 hours of TTX increased GluA1 S845 phosphorylation but not S831 phosphorylation. The Results section, “GluA1 phospho-S845 is required for scaling-up” (page unavailable), reports that TTX-induced scaling-up was eliminated in S845A knock-in neurons but remained normal in S831A neurons. (LLM, conf=0.94)
- Partly supportedcites Kim and Ziff, 2014 sourceExperimental — accuracy not yet measured
The Results section, “pGluA1(S845) Is Required for TTX-Induced Synaptic Scaling” (page unavailable), reports increased S845 phosphorylation after TTX treatment and says TTX could not induce scaling in neurons from GluA1 S845A knock-in mice. Our copy does not address whether S831 phosphorylation increases or whether scaling remains intact in S831A mutant neurons (searched: S831 phosphorylation, S831A mutant neurons). (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Bicuculline treatment stimulates GluA2 ubiquitination on K882 (Widagdo et al., 2015), very close to the Y876 and S880 phosphorylation sites, and AMPAR ubiquitination has been shown to be required for homeostatic scaling-down (Scudder et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Partly supportedcites Widagdo et al., 2015 sourceExperimental — accuracy not yet measured
The Results section reports that bicuculline induces ubiquitination of GluA2, and a separate Results section identifies K882 as a major GluA2 ubiquitination site. However, the K882 mapping used AMPA treatment, not bicuculline, so the paper does not establish that bicuculline stimulates ubiquitination specifically at K882. The scaling-down statement is cited to Scudder et al., not to Widagdo et al. (LLM, conf=0.88)
- Partly supportedcites Scudder et al., 2014 sourceExperimental — accuracy not yet measured
In the section on homeostatic downscaling (pages not supplied), the paper reports increased AMPAR ubiquitination after bicuculline treatment and shows that Nedd4-1 knockdown prevents downscaling of surface AMPARs and synaptic strength. It establishes that Nedd4-1 is required, but does not directly show that ubiquitination of AMPARs themselves is required. The GluA2 K882 claim is attributed to a different citation and is not part of this verdict. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“GluA1 undergoes dephosphorylation of T840 and S845 during LTD by protein phosphatases PP1/PP2A and CaN, respectively (Delgado et al., 2007, Toda and Huganir, 2015, Lee et al., 1998, Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Delgado et al., 2007 sourceExperimental — accuracy not yet measured
The Results sections on chem-LTD and T840 phosphatases report persistent T840 dephosphorylation during chemical LTD and show that inhibiting PP1/PP2A prevents NMDA-induced T840 dephosphorylation. They do not establish the same change during synaptically induced LTD, and the paper does not identify CaN as the phosphatase responsible for S845 dephosphorylation. (LLM, conf=0.87)
- Partly supportedcites Toda and Huganir, 2015 sourceExperimental — accuracy not yet measured
The Abstract links S845 phosphorylation changes to LTD, and the Results report that a PP1/PP2A inhibitor blocks T840 dephosphorylation after PACAP38 stimulation. The paper does not establish that PP1/PP2A dephosphorylates T840 during LTD or that CaN dephosphorylates S845 during LTD; the Discussion describes PACAP38’s possible role in LTD as conceivable and requiring further study (page numbers unavailable). (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Lee et al., 1998 source
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In the paper
“Neither GRIP1/2 nor PICK1 are required for scaling-down (Tan et al., 2015, Anggono et al., 2011).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Tan et al., 2015 source
The Discussion says that downscaling remains intact in GRIP knockout neurons and describes PICK1 as dispensable for scaling down. The results section also reports intact bicuculline-induced scaling down regardless of GRIP expression. (LLM, conf=0.93)
- Partly supportedcites Anggono et al., 2011 sourceExperimental — accuracy not yet measured
The Results report robust scaling-down after bicuculline treatment in PICK1 knockout neurons, supporting the PICK1 part of the sentence. The cited paper does not establish that GRIP1/2 are dispensable for scaling-down, so it does not support the full claim attributed jointly to the two citations. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Scaling-up appears to involve increased tyrosine phosphorylation of GluA2 as a result of downregulation of the tyrosine phosphatase, STEP61 (Figure 3), and scaling-up could be blocked by exogenously applied STEP61 (Jang et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Partly supportedcites Jang et al., 2015 sourceExperimental — accuracy not yet measured
The Results and discussion report that activity blockade reduced STEP61 and increased GluA2 tyrosine phosphorylation, and that TAT-STEP WT preincubation abolished TTX-induced synaptic scaling. However, the applied TAT-STEP protein was a STEP46 fusion, not exogenously applied STEP61 as the claim specifies. Page numbers were not provided in our copy. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Despite the fact that both GluA1 and GluA2 have been implicated in homeostatic scaling-up, complete knock-out of GluA1 still allowed for the scaling-up of GluA2/3, and complete knock-out of GluA2/3 still allowed for the scaling-up of GluA1 (Altimimi and Stellwagen, 2013), suggesting that regulatory elements in GluA1/2 can be circumvented by complete removal of these subunits.”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Altimimi and Stellwagen, 2013 source
The Results report increased GluA2 surface expression in GluA1-knockout cultures and increased GluA1 surface expression in GluA2/GluA3 double-knockout cultures after activity blockade. The Discussion states that synaptic scaling was preserved despite these constitutive deletions (article pp. 11763–11767). (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Concomitantly, GRIP1 protein is upregulated during scaling-down, but remains in intracellular compartments where it may act to sequester internalized GluA2-containing receptors away from the synapse (Figure 3) (Tan et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Partly supportedcites Tan et al., 2015 sourceExperimental — accuracy not yet measured
The section on GRIP1 subcellular distribution (Fig. 4) reports that scaling down increases cytoplasmic GRIP1 and decreases synaptic GRIP1. It describes a cytoplasmic GRIP1 pool that can retain AMPARs intracellularly, but does not show that the increased pool sequesters internalized GluA2-containing receptors during scaling down; it instead reports reduced overall GRIP1–GluA2 interaction. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Scaling-up can be blocked by the expression of the soluble cytosolic C-terminal tail of GluA2 or by shRNA-mediated knock-down of GluA2 (Gainey et al., 2009, Ancona Esselmann et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Gainey et al., 2009 source
The Results section (‘The GluR2 C-tail but not the GluR1 C-tail blocks synaptic scaling’; page not provided) reports that expression of a GluR2 C-tail peptide completely blocked scaling. The Results section on GluR2 knockdown likewise reports that shRNA-mediated knockdown prevented the TTX-induced increase in mEPSC amplitude. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Ancona Esselmann et al., 2017 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“GluA1 T840 phosphorylation has been shown to increase GluA1 single channel conductance while phosphorylation of S845 increases channel open probability, suggesting that dephosphorylation of these sites might also be important to reduce ion channel properties for expression of LTD (Banke et al., 2000, Jenkins et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Partly supportedcites Banke et al., 2000 sourceExperimental — accuracy not yet measured
The Discussion states that phosphorylation of GluR1 Ser845 increases peak open probability, supporting the S845 part of the claim. The paper does not address T840 phosphorylation or attribute increased single-channel conductance to T840; its Discussion instead associates increased unitary conductance with Ser831 phosphorylation. (LLM, conf=0.87)
- Supportedcites Jenkins et al., 2014 source
The Results report increased conductance with a Thr840 phosphomimetic mutation and increased open probability with a Ser845 phosphomimetic mutation. The Discussion interprets these findings as Thr840 phosphorylation increasing conductance and Ser845 phosphorylation enhancing open probability. The experiments used phosphomimetic substitutions rather than directly measuring both effects after phosphorylation. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“During the induction phase of LTD, transient signaling from synaptic CP-AMPARs is required for the full expression of LTD, and during the progression of LTD induction these CP-AMPARs signal their own removal through activation of calcineurin (CaN) (Sanderson et al., 2016).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Sanderson et al., 2016 source
The Discussion states that CP-AMPAR signaling during LTD induction is required for robust LTD expression and helps trigger AKAP-anchored calcineurin-mediated removal of the newly recruited receptors. The Results likewise describe calcium signaling by recruited CP-AMPARs as helping determine LTD expression before triggering their own removal. (LLM, conf=0.94)
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In the paper
“CaMKII is well known to be required for LTP, but its activity is also required during LTD where a prolonged “weak” stimulus favors the phosphorylation of GluA1 S567 over S831, leading to removal of synaptic GluA1 (Coultrap et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Supportedcites Coultrap et al., 2014 source
The Results section, “CaMKII is required for LTD,” reports that CaMKII inhibition blocked NMDAR-dependent LTD in hippocampal CA1. The Results section on differential biochemical regulation says weak, prolonged LTD-type stimuli favor GluA1 S567 over S831 phosphorylation; the Discussion says S567 phosphorylation decreases synaptic AMPAR localization. The demonstrated requirement is specifically for the NMDAR-dependent form of LTD studied here. (LLM, conf=0.91)
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In the paper
“Prolonged TTX treatment in cultured neurons causes lysosomal degradation of PICK1, while deletion of PICK1 enhances mEPSC amplitude and occludes homeostatic scaling-up, suggesting that decreased activity of PICK1 is an important mediator of scaling-up (Figure 3) (Anggono et al., 2011).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Supportedcites Anggono et al., 2011 source
In Results, “Neuronal activity regulates PICK1 protein level in cultured neurons” (Fig. 1E,F), prolonged TTX treatment reduced PICK1, and a lysosomal inhibitor largely prevented that reduction. In Results, “TTX-induced synaptic scaling is occluded in PICK1 knockout neurons” (Fig. 2A–C), knockout neurons had higher basal mEPSC amplitudes and did not show the TTX-induced scaling-up seen in wild-type neurons. The Discussion proposes that reduced PICK1 during inactivity helps promote receptor accumulation, consistent with the citing sentence’s interpretation. (LLM, conf=0.92)
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In the paper
“Homeostatic scaling-up has also been observed in the visual cortex in mice in response to visual deprivation, and involves the recruitment of synaptic CP-AMPARs and increased GluA1 S845 phosphorylation (Goel et al., 2006, Goel et al., 2011).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Not checked — no full text of the sourcecites Goel et al., 2006 source
- Supportedcites Goel et al., 2011 source
The Discussion reports that visual deprivation-induced scaling up in the mouse visual cortex was associated with increased GluR1 (GluA1) S845 phosphorylation and accompanied by synaptic incorporation of Ca2+-permeable GluR1-homomers. This supports both mechanisms attributed to the paper. (LLM, conf=0.94)
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In the paper
“TTX-induced homeostatic scaling-up in cultured neurons increases GluA1 protein expression as well as surface and synaptic levels of CP-AMPARs (GluA1 homomers) and GluA1/2 heteromers but not in GluA3-containing AMPARs (Figure 3) (Diering et al., 2014, Soares et al., 2013, Tan et al., 2015, Kim and Ziff, 2014, Hu et al., 2010).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-up
What the sources say
- Partly supportedcites Diering et al., 2014 sourceExperimental — accuracy not yet measured
The Results section, “Changes in AMPAR phosphorylation during homeostatic scaling” (page unavailable), reports that 48 hours of TTX increased surface GluA1 and GluA2 but not GluA3, consistent with GluA1/2-containing receptors rather than GluA2/3-containing receptors. Other Results passages report synaptic recruitment of GluA1 and changes in total AMPAR expression, but do not establish increased total GluA1 specifically or increased surface and synaptic levels of both GluA1 homomers (CP-AMPARs) and GluA1/2 heteromers. (LLM, conf=0.85)
- Partly supportedcites Soares et al., 2013 sourceExperimental — accuracy not yet measured
In “Homeostatic upregulation of synaptic GluA2-lacking AMPARs” (page unavailable), the paper reports increased total and surface GluA1 after TTX treatment and evidence of synaptic GluA2-lacking AMPARs in organotypic hippocampal slices. It does not establish that these receptors are specifically GluA1 homomers, that GluA1/2 heteromers increase, or that GluA3-containing AMPARs do not increase. The claim also describes cultured neurons more broadly than the slice preparation studied. (LLM, conf=0.88)
- Partly supportedcites Tan et al., 2015 sourceExperimental — accuracy not yet measured
The Results section reports that chronic TTX increased total GluA1 and surface GluA1 and GluA2, but not surface GluA3. The Discussion interprets the surface changes as preferential GluA1/GluA2 heteromer insertion. It does not establish increased surface or synaptic GluA1-homomer CP-AMPARs; instead, it says their synaptic insertion was unlikely to predominate (page numbers unavailable). (LLM, conf=0.88)
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In the paper
“Dephosphorylation of GluA2 S880 during scaling-down is mediated by activation of phosphatase PP1, through its regulatory protein inhibitor 2 (I-2) (Siddoway et al., 2013), while dephosphorylation of GluA2 Y876 requires an upregulation of STEP61 (Jang et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Supportedcites Siddoway et al., 2013 source
The Results (Fig. 3J,K) state that I-2 phosphorylation activates PP1, which dephosphorylates GluA2 at S880; blocking I-2 phosphorylation attenuated that dephosphorylation. The paper also links this pathway to synaptic downscaling. The STEP61 clause is attributed to Jang et al., not to this source. (LLM, conf=0.94)
- Partly supportedcites Jang et al., 2015 sourceExperimental — accuracy not yet measured
The Jang citation attaches to the STEP61/GluA2 Y876 clause, not the PP1/I-2 clause. In Results and discussion (page not supplied), increased STEP61 coincided with reduced phosphorylation of GluA2 at a three-tyrosine site that includes Y876. The authors say the specific GluA2 tyrosine residues regulated by STEP61 are unknown, and inhibiting STEP did not block the measured reduction in three-tyrosine phosphorylation; the paper therefore does not establish that Y876 dephosphorylation requires STEP61 upregulation. (LLM, conf=0.88)
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In the paper
“Bicuculline-induced scaling-down in cultured neurons involves the downregulation of GluA1/2/3 protein levels as well a reduced synaptic targeting of all AMPAR subunits (Diering et al., 2014, Tan et al., 2015).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Partly supportedcites Diering et al., 2014 sourceExperimental — accuracy not yet measured
The Results section, “Changes in AMPAR phosphorylation during homeostatic scaling” (page unavailable), reports that bicuculline reduced cell-surface GluA1, GluA2 and GluA3 in cultured neurons. “GluA1 phospho-S845 is required for scaling-up” mentions changes in total AMPAR expression but does not specify downregulation of all three subunits. The copy documents reduced PSD-associated GluA1, not reduced synaptic targeting of every subunit. (LLM, conf=0.85)
- Partly supportedcites Tan et al., 2015 sourceExperimental — accuracy not yet measured
The ‘Inactivity-Induced Synaptic Scaling Is Blocked in GRIP Knockout’ section reports that bicuculline reduced total GluA1, GluA2, and GluA3 expression and reduced surface levels of all three in cultured neurons (Fig. S1; Fig. 3 A–D). It does not establish reduced synaptic targeting of each subunit specifically; the reported subunit-specific measurements are of surface levels. (LLM, conf=0.84)
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In the paper
“AMPARs play an essential role in the functioning of the brain, and changes in the abundance of post-synaptic AMPARs are a fundamental mechanism for most forms of synaptic plasticity (Huganir and Nicoll, 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Concluding remarks
What the sources say
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
The Conclusions and Future Directions section says changes in AMPAR number at synaptic spines mediate changes in strength during LTP and LTD. The Proposed Working Models for LTP section calls AMPAR regulation key to many forms of synaptic plasticity and important for learning and memory, but it does not establish the claim’s stronger scope of “most forms.” Page numbers are unavailable in our copy. (LLM, conf=0.84)
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In the paper
“Thus the “slot hypothesis” offers some explanation for the prominent role of GluA1 in LTP and of GluA2 in LTD, via the rapid activity-dependent mobilization of GluA1-containing receptors onto the cell surface during LTP, and the removal of GluA2 containing receptors from the cell-surface during LTD through interactions with AP2 and/or through interactions involving the GluA2 Y-rich motif (Ahmadian”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Supportedcites Ahmadian et al., 2004 source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites Anggono and Huganir, 2012 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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In the paper
“Synaptic GluA1 is dephosphorylated at S831 and S845 during scaling-down and also in the forebrain during sleep (Diering et al., 2014, Diering et al., 2017), which together with other observations suggests that homeostatic scaling-down occurs across the forebrain during sleep (Diering et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Partly supportedcites Diering et al., 2014 sourceExperimental — accuracy not yet measured
The Results section, “Changes in AMPAR phosphorylation during homeostatic scaling” (page unavailable), reports decreased GluA1 phosphorylation at both S831 and S845 after bicuculline-induced scaling-down. It does not establish that both decreases occurred specifically in synaptic GluA1. The sleep finding is separately attributed to Diering et al. (2017), not to this source. (LLM, conf=0.82)
- Supportedcites Diering et al., 2017 source
The passage labeled Abstract describes AMPAR dephosphorylation during homeostatic scaling-down and reports decreased synaptic GluA1 phosphorylation at S845 and S831 in mouse forebrain PSD samples collected during sleep versus wake. It also says the forebrain changes were examined because they had previously been observed during scaling-down in vitro. (LLM, conf=0.91)
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In the paper
“Forms of LTP, LTD and homeostatic scaling have been shown to be intact in knock-out mice of different AMPAR subunits as well as in using molecular replacement experiments (Huganir and Nicoll, 2013, Granger et al., 2013, Ancona Esselmann et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Partly supportedcites Huganir and Nicoll, 2013 sourceExperimental — accuracy not yet measured
In “Subunit Dependence of AMPAR Trafficking and LTP and LTD” (page unavailable), the review reports that molecular replacement found no specific AMPAR-subunit requirement for LTP. “NMDAR-Dependent LTD” reports normal LTD in mice lacking GluA2/GluA3 or GluA1. The review describes homeostatic synaptic scaling in “Dynamic Regulation of AMPAR Membrane Trafficking,” but does not say it remains intact in AMPAR-subunit knockout mice or molecular replacement experiments. (LLM, conf=0.88)
- Partly supportedcites Granger et al., 2013 sourceExperimental — accuracy not yet measured
The Introduction and the section “LTP requires a reserve pool of AMPARs” report normal LTP with some molecular replacements and with GluA2 or GluA3 deletion. But the latter section reports impaired LTP after GluA1 deletion, so the knockout claim is too broad. The paper does not establish intact LTD or homeostatic scaling in these experiments. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites Ancona Esselmann et al., 2017 source
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In the paper
“GluA2-containing receptors (likely GluA2/3 heteromers) undergo spontaneous and constitutive exocytosis, but these events are much smaller, containing an estimated 2-5 receptors (Araki et al., 2010, Gu et al., 2016, Lin et al., 2009).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Partly supportedcites Araki et al., 2010 sourceExperimental — accuracy not yet measured
The Discussion reports that GluA2 exocytosis is largely constitutive (approximately 70%) and that its insertion events contain only a few receptors compared with GluA1; it also discusses GluA2/3 heteromers. The Results report lower fluorescence intensity for GluA2 events, but our copy does not give the claimed estimate of 2–5 receptors per event. (LLM, conf=0.87)
- Not matchedcites Gu et al., 2016
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Lin et al., 2009 sourceExperimental — accuracy not yet measured
In Results, under “Capturing insertion events of GluRs” (page unavailable), the paper associates GluR2 with constitutive trafficking but says it rarely observed GluR2 insertion under normal conditions. It does not identify those receptors as likely GluR2/3 heteromers or support the estimate of 2–5 receptors per event. (LLM, conf=0.86)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Interestingly, GluA1 which remains phosphorylated is resistant to scaling-down and the unphosphorylated GluA1 containing receptors are preferentially removed (Figure 4) (Diering et al., 2014).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and homeostatic scaling-down
What the sources say
- Supportedcites Diering et al., 2014 source
The Results section, “Phospho-S845 GluA1 is resistant to scaling-down,” reports that phosphorylated receptors remained on the cell surface while overall surface GluA1 decreased. The Discussion, “AMPAR phosphorylation and global synaptic plasticity,” explicitly concludes that non-phosphorylated receptors are preferentially removed and PKA-phosphorylated receptors resist scaling-down. The finding is described under conditions of high PKA activity; page numbers are not provided in our copy. (LLM, conf=0.94)
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- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“GluA2 can directly interact with AP-2 clathrin adapter complex, which allows GluA2-containing receptors to be rapidly depleted from the cell-surface (Kastning et al., 2007, Lee et al., 2002).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Supportedcites Kastning et al., 2007 source
The Results show that the GluR2 cytoplasmic tail binds directly to the μ2 subunit of AP-2. The Discussion describes rapid AP-2-dependent AMPA receptor recycling and reports that disrupting AP-2 binding increases surface GluR levels, supporting the claimed role in removal from the cell surface. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites Lee et al., 2002 source
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In the paper
“Four subunits, GluA1-4, assemble into tetramers to make up the core functional ion channel, with different combinations conferring unique cellular trafficking behaviors and biophysical characteristics (Shepherd and Huganir, 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction
What the sources say
- Not checked — no full text of the sourcecites Shepherd and Huganir, 2007 source
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In the paper
“Layers of regulation are added to AMPAR tetramers through these different interactions and modifications, increasing the computational power of synapses.”
§ The AMPA receptor code of synaptic plasticity > Abstract
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Probably not a substantial claim. The paper may give no reason why it holds.
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In the paper
“In some cases, it has been shown that certain AMPAR PTMs can influence others (Figure 1C), either by inhibiting or promoting the neighboring modification, suggesting that of all possible AMPARs variants some will be favored.”
§ The AMPA receptor code of synaptic plasticity > Introduction > Post-translational modifications of AMPAR subunits
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In the paper
“AMPAR subunits contain highly conserved ligand binding and transmembrane domains that allow glutamate binding and channel pore assembly respectively, but are divergent in their extracellular amino-terminal domains and cytoplasmic carboxy-terminal tails which are subject to PTMs (Shepherd and Huganir, 2007) (Figure 1).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Subunit combinations
What the sources say
- Not checked — no full text of the sourcecites Shepherd and Huganir, 2007 source
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In the paper
“Earlier studies suggest that long-tailed AMPARs are recruited to synapses in an activity-dependent manner, while short-tailed AMPARs undergo constitutive cycling in and out of synapses (Shi et al., 2001, Hayashi et al., 2000).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Subunit combinations
What the sources say
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The dynamic nature of AMPARs suggests that the AMPAR code will function by shifting equilibriums in favor of synaptic accumulation or removal, and by altering ion channel properties.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“recent data from Zhou et al., provide strong evidence that the GluA1 C-terminal tail is both necessary and sufficient for hippocampal LTP (Zhou et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“The result of this modification is that GluA2 containing receptors have a linear current-voltage (I-V) relationship and are impermeable to Ca2+, while GluA2-lacking receptors show high conductance and rapid decay kinetics, inward-rectification due to voltage-dependent block by intracellular polyamines and are permeable to Ca2+, thus GluA2-lacking receptors are usually referred to as calcium-perme”
§ The AMPA receptor code of synaptic plasticity > Introduction > Subunit combinations
What the sources say
- Not checked — no full text of the sourcecites Burnashev et al., 1992 source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For each type of plasticity, certain AMPAR variants will be preferentially added or removed from synapses or undergo selective changes in channel properties.”
§ The AMPA receptor code of synaptic plasticity > Introduction
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In the paper
“Incredibly, LTP was rescued in GluA1C2KI and GluA2C1KI double mutant mice, showing that the C-tail of GluA1 is sufficient for LTP expression, even when it is attached to the GluA2 subunit (Zhou et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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- Not matched
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In the paper
“As an example, GluA1 undergoes 11 known PTMs each of which can occur independently and reversibly (7 phosphorylations, 2 palmitoylations, 1 S-nitrosylation, 1 ubiquitination), allowing for 211, or 2,048 possible modified variants of GluA1”
§ The AMPA receptor code of synaptic plasticity > Introduction > Post-translational modifications of AMPAR subunits
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In the paper
“Thus, while phosphorylation of GluA1 S831 or S845 are clearly involved in LTP, the strict requirement for each site as well as the synergistic effects of dual phosphorylation are likely synapse- and induction-specific.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
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In the paper
“Importantly, LTP was completely absent in GluA1C2KI mice, demonstrating that the GluA1 C-tail is necessary for LTP.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“All four AMPAR subunits are palmitoylated at a conserved cysteine residue in the C-terminal juxtamembrane region (GluA1 C811, GluA2 C836, GluA3 C841, GluA4 C817) and a second site within the transmembrane domain TM2 (Hayashi et al., 2005).”
§ The AMPA receptor code of synaptic plasticity > Introduction > Post-translational modifications of AMPAR subunits
What the sources say
- Not checked — no full text of the sourcecites Hayashi et al., 2005 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, synaptic potentiation through GluA3 may not require AMPAR trafficking, but rather cAMP-dependent enhancement of channel open-probability of GluA3-containing receptors already localized to synapses, allowing for very rapid changes in synaptic efficacy.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTP
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This mechanism likely also applies to GluA3, which also interacts with GRIP1/2 and PICK and the phosphorylation site, S885 is conserved with GluA2 S880 (Figure 1B).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“AMPARs must be removed from the PSD, allowing for lateral diffusion away from the synapse, and concomitantly, AMPARs are locally depleted from the cell-surface by clathrin- and dynamin-dependent endocytosis (Shepherd and Huganir, 2007).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not checked — no full text of the sourcecites Shepherd and Huganir, 2007 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If PKA is not able to phosphorylate GluA1 S845, CP-AMPAR recruitment to synapses during LTD is blocked, possibly explaining the complete absence of LTD in GluA1 S845A knock-in mice.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Hippocampal LTD is still observed in knock-outs of GluA2/3 (Meng et al., 2003), but not in neurons expressing GluA2 fused to the GluA1 C-tail (Zhou et al., 2017).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not checked — no full text of the sourcecites Meng et al., 2003 source
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“GluA1 S845 dephosphorylation is critical for hippocampal LTD, as the GluA1 S845A mutation results in impaired LTD (Lee et al., 2003, Lee et al., 2010), indicating that the induction of LTD requires PKA phosphorylation of GluA1 even though receptors are eventually dephosphorylated (Huganir and Nicoll, 2013).”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Again, these findings suggest that synaptic plasticity is modulated by regulatory elements with the AMPAR C-tails, but this regulation is circumvented in the absence of AMPAR subunits.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“NMDAR-LTD can be rescued in the GluA1C2KI/GluA2C1KI double mutants, showing that the GluA2 C-tail is both necessary and sufficient for hippocampal NMDAR-LTD.”
§ The AMPA receptor code of synaptic plasticity > Introduction > The AMPAR code and LTD
What the sources say
- Not matchedcites Zhou et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During synaptic plasticity, the number of PSD slots may be altered, and/or the affinity of PSD slots for AMPARs might be changed, such that AMPARs can accumulate in the PSD during LTP and are removed during LTD (Figure 2).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the plane of the plasma membrane, AMPARs are highly mobile but become trapped in PSD slots (Opazo et al., 2012).”
§ The AMPA receptor code of synaptic plasticity > Introduction > AMPAR code and the post-synaptic density slot hypothesis
What the sources say
- Not checked — no full text of the sourcecites Opazo et al., 2012 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
AMPAR subunit combinations in brain regions outside hippocampal CA1 are largely similar to those in hippocampal CA1.
“Based on this study it has been assumed that the subunit combinations in the rest of the brain are largely similar”
The paper relies on this without support.
The majority of AMPARs in the brain are heteromers.
“Since the majority of AMPARs in the brain are heteromers”
The paper relies on this without support.
The majority of research is done during the light phase, when CP-AMPARs are less prevalent.
“As the majority of research is done during the light phase, when CP-AMPARs are less prevalent”
The paper relies on this without support.
CP-AMPARs are mostly GluA1 homomers.
“CP-AMPARs, the majority of which are likely to be GluA1 homomers”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“dopamine, norepinephrine, and serotonin signaling have all been associated with strengthening AMPAR signaling through phosphorylation and membrane insertion which likely contribute to the antidepressant effects of ketamine (Cai et al., 2013; Diering & Huganir, 2018; Hu et al., 2007; Sun et al., 2005).”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Diering & Huganir, 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“long-term potentiation (LTP), in which brief repetitive synaptic stimulation results in long-lasting increases in synaptic strength, was gaining popularity as a cellular model for learning and memory (16–22).”
From Synaptic memory and CaMKII (2023) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Although it is difficult to entirely exclude the possibility of a minor presynaptic component of NMDAR-dependent LTP, the evidence is overwhelming that its expression is primarily postsynaptic.”
From Synaptic memory and CaMKII (2023) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Thus, it is now generally accepted that LTP expression is due to the rapid postsynaptic accumulation of AMPARs.”
From Synaptic memory and CaMKII (2023) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Endocytic recycling, in which internalized surface proteins are routed back to the plasma membrane, is a key mechanism by which neurons control the composition of surface receptors, adhesion molecules, and transporters in response to synaptic activity”
From Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity (2025) · cites this paper as Diering and Huganir, 2018
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“AMPAR recycling is known to be a key source of additional receptors for LTP (Park et al., 2004; Diering and Huganir, 2018)”
From Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity (2025) · cites this paper as Diering and Huganir, 2018
Citations
Cites
Jenuwein, T., & Allis, C. D. (2001) · Science · doi:10.1126/science.1063127 · Cited by 9,756
Glutamate neurotoxicity and diseases of the nervous system
Choi, D. W. (1988) · Neuron · doi:10.1016/0896-6273(88)90162-6 · Cited by 8,188
Chen, X., Xiu, M., Xing, J., Yu, S., Min, D., & Guo, F. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000479439 · Cited by 5,760
AMPA Receptor Trafficking and Synaptic Plasticity
Malinow, R., & Malenka, R. C. (2002) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.25.112701.142758 · Cited by 2,588
Activity-dependent scaling of quantal amplitude in neocortical neurons
Turrigiano, G. G., Leslie, K. R., Desai, N. S., Rutherford, L. C., & Nelson, S. B. (1998) · Nature · doi:10.1038/36103 · Cited by 2,226
The self-tuning neuron: synaptic scaling of excitatory synapses
Turrigiano, G. G. (2008) · Cell · doi:10.1016/j.cell.2008.10.008 · Cited by 1,533
Hayashi, Y., Shi, S.-H., Esteban, J. A., Piccini, A., Poncer, J.-C., & Malinow, R. (2000) · Science · doi:10.1126/science.287.5461.2262 · Cited by 1,524
Taverna, S. D., Li, H., Ruthenburg, A. J., Allis, C. D., & Patel, D. J. (2007) · Nature Structural & Molecular Biology · doi:10.1038/nsmb1338 · Cited by 1,476
Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity
Lee, H.-K., Barbarosie, M., Kameyama, K., Bear, M. F., & Huganir, R. L. (2000) · Nature · doi:10.1038/35016089 · Cited by 1,116
Self-citationStargazin regulates synaptic targeting of AMPA receptors by two distinct mechanisms
Chen, L., Chetkovich, D. M., Petralia, R. S., Sweeney, N. T., Kawasaki, Y., Wenthold, R. J., Bredt, D. S., & Nicoll, R. A. (2000) · Nature · doi:10.1038/35050030 · Cited by 1,111
Cited by
Sorted by citations
Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988
“Many studies have shown that AMPARs also take part in the modulation of synaptic plasticity.(83,84) However, AβOs induce AMPAR ubiquitination and degradation, leading to the loss of AMPARs followed by the suppression of synaptic transmission.”
BackgroundStructure, Function, and Pharmacology of Glutamate Receptor Ion Channels
Hansen, K. B., Wollmuth, L. P., Bowie, D., Furukawa, H., Menniti, F. S., Sobolevsky, A. I., Swanson, G. T., Swanger, S. A., Greger, I. H., Nakagawa, T., et al. (2021) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000131 · Cited by 686
Glioma synapses recruit mechanisms of adaptive plasticity
Taylor, K. R., Barron, T., Hui, A., Spitzer, A., Yalçın, B., Ivec, A. E., Geraghty, A. C., Hartmann, G. G., Arzt, M., Gillespie, S. M., et al. (2023) · Nature · doi:10.1038/s41586-023-06678-1 · Cited by 378
CaM Kinase: Still Inspiring at 40
Bayer, K. U., & Schulman, H. (2019) · Neuron · doi:10.1016/j.neuron.2019.05.033 · Cited by 314
Neuromodulation of Spike-Timing-Dependent Plasticity: Past, Present, and Future
Brzosko, Z., Mierau, S. B., & Paulsen, O. (2019) · Neuron · doi:10.1016/j.neuron.2019.05.041 · Cited by 267
Metadata
- Authors
- Diering, G. H., & Huganir, R. L.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Johns Hopkins University (US)
- Corresponding author
- Huganir, Richard L.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2018-10
- Volume
- 100
- Issue
- 2
- Pages
- 314-329
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC6214363
- OpenAlex
- W2898344414
- Semantic Scholar
- c649a9fc04f1638d80f28d4badb4d2d5dd4a1cab
- Cited by
- 844
- References
- 158
- Citations by year
- 2026: 90 · 2025: 114 · 2024: 128 · 2023: 111 · 2022: 118 · 2021: 161 · 2020: 84 · 2019: 35 · 2018: 3
- FWCI
- 28.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (submittedVersion)
- PubMed Central (submittedVersion)
- Funders
- National Institute of Mental Health (P50MH100024)
- National Institute of Neurological Disorders and Stroke (R01 NS-036715)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- AMPA receptors, synaptic plasticity, long-term potentiation, long-term depression, auxiliary subunits, post-translational modification, postsynaptic receptors
- MeSH terms
- Animals, Brain, Humans, Neuronal Plasticity, Synapses, Receptors, AMPA
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-12, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-12 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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