The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index; 31 of the 80 sources its claims cite were checked for support.
AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors
Open accessAbstract
AMPA receptors (AMPARs) are tetrameric ion channels assembled from GluA1–GluA4 subunits that mediate the majority of fast excitatory synaptic transmission in the brain. In the hippocampus, most synaptic AMPARs are composed of GluA1/2 or GluA2/3 with the GluA2 subunit preventing Ca 2+influx. However, a small number of Ca 2+-permeable GluA1 homomeric receptors reside in extrasynaptic locations where they can be rapidly recruited to synapses during synaptic plasticity. Phosphorylation of GluA1 S845 by the cAMP-dependent protein kinase (PKA) primes extrasynaptic receptors for synaptic insertion in response to NMDA receptor Ca 2+signaling during long-term potentiation (LTP), while phosphatases dephosphorylate S845 and remove synaptic and extrasynaptic GluA1 during long-term depression (LTD). PKA and the Ca 2+-activated phosphatase calcineurin (CaN) are targeted to GluA1 through binding to A-kinase anchoring protein 150 (AKAP150) in a complex with PSD-95, but we do not understand how the opposing activities of these enzymes are balanced to control plasticity. Here, we generated AKAP150ΔPIX knock-in mice to selectively disrupt CaN anchoring in vivo. We found that AKAP150ΔPIX mice lack LTD but express enhanced LTP at CA1 synapses. Accordingly, basal GluA1 S845 phosphorylation is elevated in AKAP150ΔPIX hippocampus, and LTD-induced dephosphorylation and removal of GluA1, AKAP150, and PSD-95 from synapses are impaired. In addition, basal synaptic activity of GluA2-lacking AMPARs is increased in AKAP150ΔPIX mice and pharmacologic antagonism of these receptors restores normal LTD and inhibits the enhanced LTP. Thus, AKAP150-anchored CaN opposes PKA phosphorylation of GluA1 to restrict synaptic incorporation of Ca 2+-permeable AMPARs both basally and during LTP and LTD.
Overview
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Written from the paper’s full text.
TL;DR
AKAP150-anchored calcineurin is required for hippocampal LTD and constrains LTP by dephosphorylating GluA1 S845 and limiting synaptic incorporation of Ca2+-permeable, GluA2-lacking AMPA receptors. AKAP150ΔPIX knock-in mice lacking CaN anchoring show absent LTD, enhanced LTP, elevated basal S845 phosphorylation, and increased AMPAR rectification that is rescued or blocked by the Ca2+-permeable AMPAR antagonist IEM1460.
Key findings
- AKAP150ΔPIX mice lack LTD at CA1 synapses: 1 Hz LFS fEPSP slope was WT 77 ± 1% vs. ΔPIX 112 ± 9% (p = 0.01); stronger 1 Hz paired-pulse LTD was also impaired (WT 64 ± 7% vs. ΔPIX 90 ± 8%, p = 0.036).
- LTP was enhanced with 1 × 100 Hz HFS: WT 134 ± 17% vs. ΔPIX 192 ± 16% (p = 0.018), with no difference using 50 Hz; relative depotentiation was similar (WT 73 ± 3%, ΔPIX 79 ± 4%, p = 0.228).
- Basal GluA1 S845 phosphorylation was elevated in ΔPIX hippocampus (pS845/GluA1: WT 0.8 ± 0.2 vs. ΔPIX 1.4 ± 0.2, p = 0.027), and NMDA-cLTD failed to remove GluA1, PSD-95, and AKAP150 from synapses in ΔPIX cultured neurons.
- ΔPIX CA1 neurons showed increased GluA2-lacking Ca2+-permeable AMPAR activity: AMPA EPSC rectification index was WT 1.5 ± 0.2 vs. ΔPIX 5.3 ± 0.8 (p = 0.003); IEM1460 restored LTD (ΔPIX 112 ± 9% to 83 ± 4%, p = 0.014) and blocked enhanced LTP (ΔPIX 192 ± 16% to 106 ± 10%, p = 0.003).
Methods
- Generated AKAP150ΔPIX knock-in mice by homologous recombination deleting 21 bp encoding 655-PIAIIIT-661, the CaN anchoring motif, and inserting a C-terminal myc tag; used WT littermates, mostly 2–3 week old mice, and cultured postnatal day 0–2 hippocampal neurons.
- Combined extracellular field recordings in acute hippocampal slices for LTP/LTD/depotentiation; whole-cell voltage-clamp for sEPSC/mEPSC/sIPSC/mIPSC, AMPA/NMDA ratios, and AMPAR rectification with intracellular spermine; biochemistry including fractionation, immunoprecipitation, and immunoblotting for pS845/GluA1; immunohistochemistry, Golgi staining, and imaging.
- Statistical comparisons used one-way ANOVA with Dunnet’s post hoc, two-way ANOVA with Bonferroni post hoc, or Student’s t-test; significance was p < 0.05, with data as mean ± SEM.
Limitations
- The paper does not include a dedicated limitations section. It notes that AMPA/NMDA ratio measurements without intracellular polyamines may underestimate changes in AMPAR subunit composition because endogenous polyamines can dialyze out during whole-cell recording.
- The paper discusses age-dependent differences, noting that findings in ~2–3 week old mice may not generalize to older ages, since prior studies show age-dependent roles for AKAP150-anchored PKA and GluA2-lacking AMPARs in LTP.
- Evident from the text: experiments used mice on a mixed C57Bl6/129 background and young animals, and no behavioral or cognitive outcomes are reported, so learning/memory effects are not tested here.
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Claims the paper makes
48 Own result · 27 Own interpretation · 16 Partly supported · 9 No full text of the sources · 5 Supported · 5 Not checked yet · 4 Sources not found · 3 Own method · 1 Supported so far · 1 Not supported · 1 No basis given · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Through its linkage by PSD-95 family MAGUKs (Colledge et al., 2000), AKAP150-anchored CaN is targeted near the C-termini of AMPARs and NMDARs, where it is optimally positioned to respond to NMDAR Ca2+ influx during LTD induction.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Disputedcites Colledge et al., 2000 sourceExperimental — accuracy not yet measured
The paper supports a linkage between AKAP79/150 and PSD-95 family MAGUKs, but not the claimed targeting of AKAP150-anchored calcineurin (CaN) through that linkage. Its Discussion (page unavailable) reports that PSD-95 competes with calcineurin for AKAP79/150 binding and suggests that MAGUK-bound AKAP79/150 preferentially targets kinases, not phosphatases, to glutamate receptors. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
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.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This AKAP removal from synapses is caused by inhibition of N-terminal targeting interactions through depalmitoylation, phospholipase C cleavage of PIP2, and CaN-dependent actin depolymerization”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
What the sources say
- Partly supportedcites Gomez et al., 2002 sourceExperimental — accuracy not yet measured
The section on reorganization of dendritic spine F-actin reports that CaN-associated actin remodeling is likely to untether AKAP79/150 from the postsynaptic cytoskeleton, and that stabilizing F-actin prevents its NMDA-mediated redistribution. The section on the AKAP79 N-terminal basic domain describes binding to PI-4,5-P2, but does not show that depalmitoylation or phospholipase C cleavage of PIP2 causes AKAP removal. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Not matchedcites Horne and Dell'Acqua, 2007
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Keith et al., 2012 source
The Results section on NMDA-LTD reports that depalmitoylation promotes AKAP79/150 removal from dendritic spines, alongside PLC-catalyzed PI4,5P2 hydrolysis and CaN-dependent F-actin reorganization. The Introduction identifies the N-terminal domain’s lipid and F-actin binding as targeting interactions disrupted during spine removal. The supplied passages do not specify page numbers. (LLM, conf=0.91)
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.
- 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
“Our findings of impaired LTD and enhanced LTP with AKAP-CaN anchoring disruption are similar to previous studies using less-specific genetic or pharmacologic inhibition of CaN activity in hippocampal slices”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion
What the sources say
- Not matchedcites Wang and Kelly, 1996, 1997
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Malleret et al., 2001 source
- Supportedcites Zeng et al., 2001 source
The Introduction (page unavailable) describes a forebrain-specific calcineurin knockout studied at hippocampal Schaffer collateral–CA1 synapses. It reports diminished LTD and modestly enhanced LTP at some stimulation frequencies, matching the comparison to genetic inhibition. The paper did not test pharmacologic inhibition, and LTP at 100 Hz was normal. (LLM, conf=0.90)
plaincorrelational- 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.
- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“a previous overexpression study in cultured rat neurons found that an AKAP150 mutant with a larger deletion surrounding the CaN anchoring site moved from spines with 100 μM NMDA treatment”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
What the sources say
- Supportedcites Bhattacharyya et al., 2009 source
The Results (PP2B binding to AKAP is required for AMPAR endocytosis; page unavailable) describe overexpression of AKAP150ΔPP2B, which deletes residues 613–655 encompassing the calcineurin-binding sequence. The Results (Loss of synaptic PSD-95 and AKAP during NMDAR activation; page unavailable) show that this mutant moved away from synapses after NMDA application. The Methods identify the neurons as rat hippocampal cultures, and the Results specify 100 μM NMDA as the treatment used in subsequent experiments. (LLM, conf=0.91)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Our findings are also in agreement with previous studies in culture preparations that implicated AKAP79/150-CaN anchoring in regulation of AMPAR activity and endocytosis underlying LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion
What the sources say
- Partly supportedcites Tavalin et al., 2002 sourceExperimental — accuracy not yet measured
The Results report that disrupting kinase anchoring reduced AMPA receptor currents in cultured hippocampal neurons, and the Discussion links AKAP79/150-anchored PP2B regulation to properties of LTD. The Discussion discusses AMPA receptor endocytosis as a possible related mechanism, but does not establish that AKAP79/150–PP2B anchoring regulates endocytosis underlying LTD. No page numbers are available in our copy. (LLM, conf=0.85)
- Partly supportedcites Hoshi et al., 2005 sourceExperimental — accuracy not yet measured
The Results (page unavailable) show that AKAP79/150 anchoring of PP2B (calcineurin) is required for downregulation of AMPA currents in cultured rat hippocampal neurons. Our copy does not show that this anchoring regulates AMPAR endocytosis or demonstrate that the observed current changes underlie LTD. (LLM, conf=0.88)
- Supportedcites Bhattacharyya et al., 2009 source
The Results section (‘PP2B binding to AKAP is required for AMPAR endocytosis’) reports that deleting AKAP150’s calcineurin-binding sequence nearly blocked NMDAR-triggered AMPAR endocytosis in cultured neurons. The Discussion links this trafficking to LTD and proposes that AKAP150 positions calcineurin to regulate it; the claim appropriately says the study implicated this mechanism rather than proved every step. (LLM, conf=0.90)
plaincorrelational- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In particular, NMDA-cLTD activation of CaN and PP1/2A negatively regulates PSD-95 postsynaptic clustering and binding to Stargazin to promote AMPAR removal”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Partly supportedcites Colledge et al., 2003 sourceExperimental — accuracy not yet measured
The Discussion reports that NMDA receptor activation triggers PSD-95 ubiquitination and removal from synaptic sites, potentially allowing AMPA receptor endocytosis. The paper also reports that inhibiting PP2B (calcineurin) prevents NMDA-induced PSD-95 loss, and the Introduction notes that PSD-95 binds stargazin. It does not show that PP1/PP2A mediate this process or that NMDA stimulation reduces PSD-95’s binding to stargazin. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Tomita et al., 2005 source
- Not checked — no full text of the sourcecites Kim et al., 2007 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We did not see enhanced induction or expression of LTP in ΔPIX mice using weaker stimuli of 50 Hz or 10 Hz that enhance potentiation in conditional CaN knockout mice (Zeng et al., 2001) and GluA1 S831,845D mice that mimic constitutive GluA1 phosphorylation”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Partly supportedcites Zeng et al., 2001 sourceExperimental — accuracy not yet measured
The passage headed “Impaired LTD But Normal LTP and Depotentiation at the Schaffer Collateral-CA1 Synapse” reports slight potentiation at 10 Hz and greater LTP at 40 Hz in conditional calcineurin knockout mice than in controls. It does not report a 50 Hz test, so the cited paper supports the comparison at 10 Hz but not the specified 50 Hz frequency. The statement about ΔPIX mice is the citing authors’ own result, not a finding attributed to this source. (LLM, conf=0.88)
- Supportedcites Makino et al., 2011 source
The Results report that 10-Hz stimulation produced long-lasting potentiation in GluA1DD mice but not wild-type mice. The paper identifies GluA1DD as the S831D/S845D phosphomimetic knock-in; the citing authors’ finding in ΔPIX mice is their own result, not a finding attributed to this source. (LLM, conf=0.91)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“peptide-mediated inhibition of PKA anchoring or activity caused a very similar decrease in AMPAR currents in hippocampal neurons that was mediated by CaN activation in part by Ca2+ influx through Ca2+-permeable AMPARs”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Not checked — no full text of the sourcecites Rosenmund et al., 1994 source
- Partly supportedcites Tavalin et al., 2002 sourceExperimental — accuracy not yet measured
In “Results: PP2B underlies rundown of hippocampal AMPA receptor current” (page unavailable), the Ht31 peptide disrupts PKA anchoring and reduces currents in cultured hippocampal neurons; cyclosporin A prevents that rundown. The authors suggest that calcium entry through calcium-permeable AMPA receptors may contribute to its initial phase. The passage describing peptide inhibition of PKA activity with PKI concerns reconstituted receptors in HEK293 cells, not hippocampal neurons, so the claim extends that part of the finding to a different cell type. (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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This finding is consistent with several earlier studies using a variety of different protocols to induce LTP that have in general observed recruitment of GluA2-lacking AMPARs in WT rodents <2 weeks-old and >4 weeks-old but not in the ~3 week-old age range that we studied”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Not checked — no full text of the sourcecites Plant et al., 2006 source
- Not matchedcites Lu et al., 2007
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Yang et al., 2010 sourceExperimental — accuracy not yet measured
The Discussion (page not supplied) reports recruitment of GluR2-lacking AMPARs during some forms of LTP and says induction protocols may account for differing findings. It does not establish the claimed age pattern: recruitment below two weeks and above four weeks, but not around three weeks. The Materials and Methods (page not supplied) specify experiments in P13–P18 rats, not comparisons across those age ranges. (LLM, conf=0.86)
hedgedcorrelational- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we evaluated presynaptic function and short-term plasticity by measuring paired-pulse facilitation ratios (PPR), and found no significant differences in PPR at SC-CA1 synapses between ΔPIX and WT over a range of inter-pulse intervals”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Basal synaptic transmission is normal in AKAP150ΔPIX knock-in mice
plainn = 9- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
- Probably not a substantial claim. 10
- It may state two separate claims as one. 50
- The quote only partly states this claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Phosphorylation of AMPAR GluA1 (formerly GluR1) subunits on S845 by PKA increases channel open probability and promotes receptor recycling and exocytosis at extrasynaptic sites near the postsynaptic density (PSD)”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Introduction
What the sources say
- Partly supportedcites Banke et al., 2000 sourceExperimental — accuracy not yet measured
The Discussion reports that PKA phosphorylation of GluR1 Ser845 appears to increase peak channel open probability. The paper does not establish the additional claim that this phosphorylation promotes receptor recycling or exocytosis at extrasynaptic sites near the PSD; the passages on receptor localization discuss it only as background. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites Ehlers, 2000 source
- 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.
Probably not a substantial claim. 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
“In cultured rat hippocampal neurons, Ca2+, CaN activity, and the AKAP79/150 CaN anchoring domain are required for the down-regulation of AMPAR currents and internalization of AMPAR in response to either acute NMDA receptor activation or inhibition of PKA anchoring and activity”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates NMDA-cLTD GluA1 dephosphorylation and removal from synapses
What the sources say
- Not checked — no full text of the sourcecites Beattie et al., 2000 source
- Partly supportedcites Tavalin et al., 2002 sourceExperimental — accuracy not yet measured
The Results section reports that disrupting PKA anchoring reduced AMPA receptor currents in cultured hippocampal neurons, and that removing extracellular calcium or inhibiting PP2B prevented this rundown. It does not establish that the AKAP79/150 PP2B-anchoring domain is required in those neurons, or show AMPA receptor internalization. NMDA receptors were blocked during the current recordings, rather than acutely activated. Page numbers are unavailable in our copy. (LLM, conf=0.89)
- Partly supportedcites Hoshi et al., 2005 sourceExperimental — accuracy not yet measured
The Results report that, in cultured rat hippocampal neurons, AKAP150 silencing abolished glutamate-dependent attenuation of AMPA currents and that rescue required the PP2B (calcineurin) anchoring site. They also report that inhibiting PKA activity with PKI induced AMPA-current downregulation. The passages do not establish a requirement for Ca2+ or calcineurin activity, or show AMPAR internalization or a response specifically to acute NMDA receptor activation. (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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“hippocampal slices from AKAP150 knockout mice exhibit normal LTD and LTP under the same conditions where AKAP150D36 mice show strong deficits in both LTP and LTD, suggesting that simultaneous removal of both PKA and CaN anchoring allows compensation”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Generation and characterization of CaN-anchoring deficient AKAP150ΔPIX knock-in mice
What the sources say
- Supportedcites Weisenhaus et al., 2010 source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“LTD-associated loss of AKAP-PKA complexes from spines and the PSD is coincident with, but slightly delayed in time from GluA1 S845 dephosphorylation and endocytosis, and may prevent re-phosphorylation of GluA1”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
What the sources say
- Supportedcites Smith et al., 2006 source
The Discussion (page not provided) says AKAP79/150 and PKA redistribution slightly lags GluR1-Ser845 dephosphorylation and internalization. The Abstract and Discussion propose that loss of these complexes could help maintain GluR1 dephosphorylation, consistent with the claim’s hedged suggestion about preventing re-phosphorylation. (LLM, conf=0.90)
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
“in ~2–3 week-old mice, where synaptic plasticity is normal in AKAP150 knockouts (Weisenhaus et al., 2010), our characterization of AKAP150ΔPIX mice revealed that CaN anchoring is essential for LTD and constrains LTP”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion
What the sources say
- Partly supportedcites Weisenhaus et al., 2010 sourceExperimental — accuracy not yet measured
The citation supports the knockout comparison, not the citing authors’ subsequent finding about AKAP150ΔPIX mice. The Results and Figure 5 report normal LTD in AKAP5 knockout mice at 10–14 days, but normal LTP was measured in 7–12-week-old mice; the paper does not establish that both forms of plasticity are normal at ~2–3 weeks (no page numbers provided). (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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“CaN is anchored within 10 nm of PKA on the AKAP (Oliveria et al., 2003), likely allowing this kinase-phosphatase pair to precisely balance each other in regulation of substrates such as GluA1 S845.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Supportedcites Oliveria et al., 2003 source
The Results section describes CaN and PKA binding sites on AKAP79, and the Discussion reports FRET measurements showing that PKA-RII and CaNA are simultaneously bound within approximately 50 Å (5 nm) of each other. This supports the proximity claim to which the citation is attached; the subsequent statement about balancing substrate regulation is the citing authors’ inference. (LLM, conf=0.94)
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 cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LTD leads to loss of AKAP79/150 binding to PSD-95 and cadherins and removal of the AKAP and PKA from synapses”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
What the sources say
- Partly supportedcites Gomez et al., 2002 sourceExperimental — accuracy not yet measured
The section on AKAP79/150–PKA association with PSD-MAGUKs reports that NMDA treatment disrupts those complexes, while the section on pathways shared with LTD describes NMDA-triggered removal of the AKAP79/150–PKA complex from synapses. The paper connects these findings to LTD-related signaling, but does not show that LTD itself causes them; the passages do not establish loss of binding to cadherins. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Gorski et al., 2005 source
- Partly supportedcites Smith et al., 2006 sourceExperimental — accuracy not yet measured
The Results section on PKA redistribution reports that chem-LTD treatment reduces AKAP150 and PKA at the postsynaptic density. The Introduction says disruption of AKAP79/150 binding to PSD-95 and cadherins was observed after stronger NMDA treatments than those needed to induce LTD; this paper does not establish that the binding loss occurs under its LTD-inducing conditions. (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
“AKAP79/150 is targeted to dendritic spines and the PSD by an N-terminal basic region that is palmitoylated on two Cys residues and binds directly to the membrane lipid phosphatidylinositol-4,5-bisphosphate (PIP2), the actin cytoskeleton, and cadherin adhesion molecules”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
What the sources say
- Not matchedcites Dell'Acqua et al., 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Gomez et al., 2002 sourceExperimental — accuracy not yet measured
The Results section reports that the AKAP79 N-terminal basic domain targets dendritic spines and binds F-actin; it also identifies PI-4,5-P2-binding basic regions. The same section attributes palmitoylation sites to PSD-95, not AKAP79, and the passages do not support binding to cadherin adhesion molecules. No page numbers are available in our copy. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Gorski et al., 2005 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“our recent published findings indicated that AKAP79/150 palmitoylation targets it to dendritic recycling endosomes in cultured neurons to specifically control GluA1 trafficking and Ca2+-permeable AMPAR synaptic activity”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Supportedcites Keith et al., 2012 source
The Abstract states that palmitoylation targets AKAP79/150 to dendritic recycling endosomes and describes experiments in cultured rat hippocampal neurons. The Results sections report that palmitoylation is required for GluR1 (GluA1) surface delivery during chemical LTP and limits basal synaptic activity of GluR2-lacking, Ca2+-permeable AMPARs. Page numbers are not available in our copy. (LLM, conf=0.91)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“GluA1 phosphorylation directly regulates trafficking, but there are other phosphatase substrates, including PSD-95 and Stargazin, that are also involved in synaptic AMPAR removal during LTD.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Partly supportedcites Colledge et al., 2003 sourceExperimental — accuracy not yet measured
The Discussion and the section on PSD-95 ubiquitination link PSD-95 to NMDA-induced AMPA receptor removal, and the paper reports that proteasome inhibitors block LTD (page numbers unavailable). It suggests PP2B may participate in PSD-95 degradation, but does not establish PSD-95 as a direct phosphatase substrate; the Introduction mentions stargazin in AMPA receptor targeting, not as a phosphatase substrate involved in receptor removal during LTD. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Tomita et al., 2005 source
- Not checked — no full text of the sourcecites Kim et al., 2007 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
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“While LTD and depotentiation are sensitive to genetic manipulations of CaN and PKA expression, their underlying signaling mechanisms are distinct”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Partly supportedcites Brandon et al., 1995 sourceExperimental — accuracy not yet measured
The Abstract reports that mice lacking the PKA RIβ subunit have severe deficits in both LTD and depotentiation, supporting sensitivity to a genetic manipulation of PKA. Our copy does not report a genetic manipulation of calcineurin (CaN) or establish that LTD and depotentiation have distinct underlying signaling mechanisms; its statement about different forms of plasticity concerns LTD/depotentiation versus LTP. (LLM, conf=0.86)
- Partly supportedcites Zhuo et al., 1999 sourceExperimental — accuracy not yet measured
The Discussion says genetic studies of PKA implicate its signaling pathway in both LTD and depotentiation, and that the two processes have distinct mechanisms. But the Results report that LTD was normal in calcineurin Aα-deficient mice while depotentiation was impaired, so the paper does not support saying both are sensitive to that genetic manipulation of calcineurin. (LLM, conf=0.87)
- Not matchedcites Yang et al., 2009
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“past work in heterologous cells demonstrated that negative regulation of recombinant GluA1 currents by AKAP79 involved dephosphorylation of S845 but not S831, required anchored CaN, and was opposed by anchored PKA”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Not matchedcites Dell'Acqua et al., 2002
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Tavalin et al., 2002 source
The GluR1 site-mutant results show that AKAP79-dependent current rundown occurs at Ser845, not Ser831. The HEK293-cell experiments identify AKAP79-associated PP2B (calcineurin) as required for rundown, while the anchored-PKA section reports that activating anchored PKA prevents it. Page numbers are unavailable in our copy. (LLM, conf=0.91)
- Partly supportedcites Hoshi et al., 2005 sourceExperimental — accuracy not yet measured
The Results (page unavailable) show that recombinant GluR1 currents run down in HEK293 cells and that loss of PP2B (calcineurin) anchoring prevents this rundown. They also link anchored PKA to Ser 845 phosphorylation and, in hippocampal neurons, to maintaining AMPA currents. The paper does not demonstrate that the current reduction specifically involves dephosphorylation of Ser 845 rather than Ser 831, or establish PKA's opposing effect in the heterologous-cell experiments. (LLM, conf=0.86)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
“In addition, forebrain-specific CaN knockout mice, like our ΔPIX mice, exhibit a lack of LTD but maintain normal depotentiation”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Partly supportedcites Zeng et al., 2001 sourceExperimental — accuracy not yet measured
The Introduction and the passage headed “Impaired LTD But Normal LTP and Depotentiation at the Schaffer Collateral-CA1 Synapse” report diminished, not absent, LTD in the knockout mice. The depotentiation passage reports comparable responses in mutant and control slices. No page numbers are available in our copy. (LLM, conf=0.88)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CaN activity is also required for cLTD-induced F-actin depolymerization and subsequent disruption of AKAP150 binding to PSD-95 and membranes (Gomez et al., 2002); this uncoupling of AKAP150 from PSD-95 and membranes may prevent PKA re-phosphorylation of GluA1 that would promote recycling after LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Partly supportedcites Gomez et al., 2002 sourceExperimental — accuracy not yet measured
In ‘Activation of the phosphatase calcineurin but not protein kinases is necessary for NMDA receptor regulation of AKAP79/150 targeting’ (page unavailable), calcineurin inhibitors mostly prevented NMDA-induced AKAP79/150 redistribution. The F-actin results and the ‘pathways shared with LTD’ discussion (pages unavailable) support a proposed sequence of actin remodeling, loss of association with PSD-95, and membrane release. The paper studied glutamate/NMDA-treated neurons rather than directly demonstrating this sequence during cLTD; the GluA1 recycling proposal follows the citation and is not attributed to this source. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites Ehlers, 2000 source
- Not checked — no full text of the sourcecites Snyder et al., 2005 source
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.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“observed no differences in spine morphology or number as quantified by spine density counts”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Generation and characterization of CaN-anchoring deficient AKAP150ΔPIX knock-in mice
plainn = 12- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both WT and ΔPIX slices exhibited depotentiation; however, while the fEPSP responses for WT slices returned to near the pre-LTP baseline after LFS, the responses in ΔPIX slices remained increased above baseline”
- Also stated in: § AKAP150-anchored CaN limits LTP but is not strictly required for synaptic depotentiation · plain
“we renormalized the last 10 minutes of the LTP responses back to baseline, and found that the relative amount of depotentiation was similar for AKAP150ΔPIX and WT”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits LTP but is not strictly required for synaptic depotentiation
plainn = 5- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
- Also stated in: § AKAP150-anchored CaN limits LTP but is not strictly required for synaptic depotentiation · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Using standard 1 Hz LFS, we found that LTD was readily detectable in WT but absent in ΔPIX mice”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN is required for LTD
plainn = 10- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we studied GABA-mediated sIPSC and mIPSC (Fig. 4A) events and found no significant differences in mean peak amplitudes or mean frequency”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Basal synaptic transmission is normal in AKAP150ΔPIX knock-in mice
plainn = 17- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we found no significant differences in action-potential dependent AMPAR-mediated spontaneous activity (sEPSCs) or action-potential independent mEPSCs for either mean peak amplitude or mean frequency”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Basal synaptic transmission is normal in AKAP150ΔPIX knock-in mice
plainn = 14- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“WT slices showed an initial decrease in fEPSP slope that was not seen for ΔPIX slices using either 10 Hz”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN is required for LTD
plainn = 10- 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.
The quote only partly states this claim.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“by 60 minutes after cLTD, S845 phosphorylation recovered completely back to the higher initial level for ΔPIX while remaining ~20% decreased for WT”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates NMDA-cLTD GluA1 dephosphorylation and removal from synapses
plainn = 6- 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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
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
“AKAP150ΔPIX mice have no obvious alterations in physical, behavioral, or breeding phenotype in the home cage environment.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Materials and Methods > Generation of AKAP150ΔPIX knock-in mice
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“revealed an expected linear I–V curve for WT neurons, consistent with the presence of GluA2 in most synaptic receptors, while ΔPIX neurons exhibited clear inward rectification in the I–V curve, with significantly decreased outward current measured at +40 mV compared to inward current at −65 mV”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain LTP
boostedcorrelationaln = 10- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While WT CA1 neurons typically displayed robust outward +40 mV and inward −65 mV AMPAR EPSCs, ΔPIX CA1 neurons in general showed reduced outward compared to inward AMPAR currents, with some neurons showing particularly large differences”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain LTP
plaincorrelationaln = 10- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“AKAP150ΔPIX required a 70 μM NMDA-cLTD treatment to remove it from synapses, whereas AKAP150WT was efficiently removed by 30 or 50 μM NMDA”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates removal of PSD-95 and AKAP150 from synapses following NMDA-LTD
plaindirectn = 16- 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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When AKAP150-CaN anchoring was disrupted in ΔPIX mice, we observed enhanced LTP expression immediately after induction with 1x100 Hz HFS as well as continued enhanced potentiation that was blocked by the Ca2+-permeable AMPAR antagonist IEM1460.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
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 result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Interestingly, in ΔPIX mice we found that LFS-LTD was impaired, but the same LFS protocol significantly depotentiated the enhanced LTP.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
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 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 S845/831A and S845A knock-in mice are deficient in LTD, but S831A mice express normal LTD, further indicating that LTD requires regulation of only S845 phosphorylation”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates NMDA-cLTD GluA1 dephosphorylation and removal from synapses
What the sources say
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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, ΔPIX deletion of 655PIAIIIT661 from AKAP150 selectively eliminates CaN anchoring while leaving intact all the other AKAP structural domains and functions including PKA and PKC anchoring, membrane targeting, ion channel binding, and linkage to AMPAR and NMDAR by PSD-95 family membrane-associated guanylate kinase (MAGUK) scaffold proteins”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Generation and characterization of CaN-anchoring deficient AKAP150ΔPIX knock-in mice
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.
- Rests on an assumption: The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
- The authors state this as an assumption: The role of AKAP150-anchored CaN in regulating LTP or LTD in vivo and the underlying mechanisms are not sufficiently understood.
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
“Brief bath application of NMDA produces a form of chemical LTD (cLTD) that is similar to homosynaptic LTD induced by LFS”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates NMDA-cLTD GluA1 dephosphorylation and removal from synapses
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This motif is required for cellular anchoring of CaN and its deletion eliminates functional regulation of L-type voltage-gated Ca2+ channel currents and signaling to the nucleus by CaN in cultured neurons”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > Generation and characterization of CaN-anchoring deficient AKAP150ΔPIX knock-in mice
What the sources say
- Not checked — no full text of the sourcecites Oliveria 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.
None of the sources cited for this claim have been checked yet.
In the paper
“while protein phosphatases PP1, PP2A, and CaN (also known as PP2B) dephosphorylate GluA1 S845 and remove receptors by endocytosis during LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Introduction
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.
Probably not a substantial claim.
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
“both of these stimulation methods induce selective dephosphorylation of GluA1 S845, but not S831, through activation of CaN and other phosphatases”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN regulates NMDA-cLTD GluA1 dephosphorylation and removal from synapses
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.
In the paper
“In contrast, IEM1460 had no effects on LTD expression in WT slices, indicating that GluA2-lacking receptors are either prevented from entering the synapse or are quickly removed by LTD induction as in He et al., 2009.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
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.
hedged- 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
None of the sources cited for this claim have been checked yet.
In the paper
“Many of these GluA1 receptors may be phosphorylated by PKA prior to LTD induction (Kameyama et al., 1998; Snyder et al., 2005); however, there is evidence that acute activation of AKAP150 anchored-PKA signaling is also required during LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
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.
None of the sources cited for this claim have been checked yet.
In the paper
“dephosphorylation and endocytosis of this pool of GluA1 is required for LTD, explaining why S845A knock-in mice that lack this receptor pool are deficient in LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain 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 checked — no full text of the sourcecites Lee et al., 2010 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.
- 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
“the enhanced basal S845 phosphorylation and impaired dephosphorylation and removal of GluA1 we observe for ΔPIX mice could indicate that there is increased synaptic contribution of Ca2+-permeable AMPAR that interfere with LTD expression”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain LTP
hedgedconditionaln = 9- 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
“these AMPA/NMDA ratio results suggest that ΔPIX mice may have more Ca2+-permeable AMPARs that increase synaptic inward currents at −65 mV with little impact on outward currents at +40 mV, which are carried predominantly by GluA2-containing receptors”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain 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.
None of the sources cited for this claim have been checked yet.
In the paper
“LTD is impaired in GluA1-S845A knock-in mice (Lee et al., 2010), where it was found that S845 phosphorylation stabilizes GluA1 homomers in extrasynaptic locations where they exchange in and out of the synapse but are removed by LTD”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during LTD
What the sources say
- Not checked — no full text of the sourcecites Lee et al., 2010 source
- Not matchedcites He et al., 2009
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.
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
“Using this integrated approach we discovered a novel role for AKAP-CaN in dephosphorylating GluA1 S845 and limiting the synaptic incorporation of GluA2-lacking Ca2+-permeable AMPARs to regulate not only LTD, but also LTP expression.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion
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
“These whole-cell recording results all point to increased activity of GluA1 homomers inΔPIX CA1 neurons that could be contributing to LTP enhancement and LTD impairment if these receptors were recruited to synapses and not removed after HFS and LFS, respectively.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain 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
“In contrast, for ΔPIX neurons, GluA2-lacking receptors are not removed and likely replace any synaptic GluA2-containing receptors removed during LTD induction to block subsequent expression.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during 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.
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
“These findings further indicate that AKAP150-CaN promotes GluA1 homomer removal, but removal of at least some GluA2-containing receptors does not strictly require CaN anchoring.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during 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
“The inward rectification of GluA2-lacking receptors is due to voltage-dependent block of the channel pore at depolarized membrane potentials by intracellular polyamines”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain LTP
What the sources say
- Not checked — no full text of the sourcecites Rozov et al., 1998 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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“During LTD, S845 is dephosphorylated by activation of CaN, PP1 and PP2A, removed from synapses, and endocytosed from the extrasynaptic membrane”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN regulation of AMPAR phosphorylation and subunit composition during 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
“based on the increased average rectification index they may have either been partially replaced by GluA2-lacking receptors at most synapses or perhaps more completely replaced at a subset of synapses”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN limits synaptic activity of GluA2-lacking Ca2+-permeable AMPA receptors to promote LTD and constrain LTP
hedgedconditionaln = 11- 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This knock-in minimized problems associated with complete AKAP150 knockout, which simultaneously removes multiple and opposing functions (i.e. both PKA and CaN anchoring) and thus limits phenotypic impacts and mechanistic interpretations.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion
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.
In the paper
“In particular, 1 x 100 Hz LTP requires PKA activity, recruits GluA2-lacking AMPARs, and is impaired in PKA-anchoring deficient AKAP150D36 mice that are >8 weeks-old but not 3–4 weeks-old”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Not matchedcites Lu et al., 2007
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
“These findings reinforce that AKAP150-CaN is very specifically targeted to regulate S845, and suggest that the amount of LTP that is refractory to depotentiation in ΔPIX mice is likely due to an inability to dephosphorylate S845 and fully suppress the activity of IEM-sensitive GluA2-lacking receptors that are aberrantly recruited during LTP.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
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
“These differences could be due to age differences; CaN knockout and S831,845D mice were studied at older ages of 4–6 weeks.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Thus, at the younger age AKAP-CaN may not only oppose PKA anchored to AKAP150, but also other pools of PKA and perhaps other kinases to limit LTP expression.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Thus, while AKAP150-anchored CaN is clearly involved in S845 dephosphorylation in LTD, it may be redundant with other phosphatase pathways that dephosphorylate S831 during depotentiation.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
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
“Nonetheless, our current results could also indicate that AKAP anchored-CaN plays a more important role in limiting the strength of potentiated response after LTP by opposing phosphorylation of S845 and regulating AMPAR subunit composition rather than in setting the induction threshold, which may involve other pools of CaN and additional substrates.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
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
“Thus, these earlier studies hinted at a role for AKAP79/150-anchored CaN in regulation of Ca2+-permeable GluA1 homomers that our results here now clearly establish as a key mechanism that maintains bi-directional synaptic plasticity in the hippocampus.”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
boosteddirect- 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
“LTD causes dephosphorylation of the GluA1 S845 PKA site, while depotentiation triggers dephosphorylation of the GluA1 S831 CaMKII/PKC site”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Discussion > AKAP150-CaN constrains the potentiated response following LTP induction by limiting synaptic incorporation of Ca2+-permeable AMPAreceptors
What the sources say
- Not checked — no full text of the sourcecites Lee et al., 2000 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 paper relies on this without support.
The C-terminal myc epitope tag introduced into AKAP150ΔPIX does not alter AKAP150 function or the phenotype.
“inserts a C-terminal myc epitope tag”
“Expression of AKAP150ΔPIX protein in homozygous mice was confirmed by immunoblotting to detect the engineered C-terminal myc tag”
The authors state this as an assumption.
The role of AKAP150-anchored CaN in regulating LTP or LTD in vivo and the underlying mechanisms are not sufficiently understood.
“However, we do not know if AKAP150-anchored CaN regulates LTP or LTD in vivo or understand the underlying mechanisms in sufficient detail.”
The paper relies on this without support.
IEM1460 selectively blocks Ca2+-permeable AMPARs without affecting other synaptic receptors.
“we applied IEM1460, an extracellular polyamine blocker of Ca2+-permeable AMPARs”
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 cited source says what the claim attributes to it.
In the citing paper
“We next tested an acute 5-minute activation of NMDARs, known to induce a sustained depression of synaptic strength20,21.”
From A trans-synaptic nanocolumn aligns neurotransmitter release to receptors (2016) · cites this paper as [21]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN is required for LTD
“Fig. 5A-B; %baseline fEPSP slope: WT 77 ± 1%, n=5; ΔPIX 112 ± 9%, n=10 slices, **p = 0.01 at t = 86 min (56 min post-LTD induction)”
§ AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors > Results > AKAP150-anchored CaN is required for LTD
“Fig. 5A; %baseline fEPSP slope: WT 74 ± 11%, n=5; ΔPIX 104 ± 10%, n=10, *p= 0.04, at 36 minutes, 1 minute post-LTD induction”
Citations
Cites
Dudek, S. M., & Bear, M. F. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.10.4363 · Cited by 1,708 · cited 1×
“…synapses in forebrain-restricted, conditional CaN knock-out mice and inhibition of LTD by CaN phosphatase inhibitors using a standard low-frequency stimulation (LFS) LTD induction protocol (900 pulses at 1 Hz) (Dudek and Bear, 1992; Mulkey and Malenka, 1992; Mulkey et al., 1994; Zeng et al., 2001).”
MethodShankar, G. M., Bloodgood, B. L., Townsend, M., Walsh, D. M., Selkoe, D. J., & Sabatini, B. L. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4970-06.2007 · Cited by 1,592 · cited 1×
“…CA1 synapses are widely studied due to their involvement in learning and memory processes that are impaired in disorders including schizophrenia, Down syndrome, and Alzheimer’s (Siarey et al., 1999; Miyakawa et al., 2003; Hsieh et al., 2006; Shankar et al., 2007; Scott-McKean and Costa, 2011).”
BackgroundRegulation 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 · cited 3×
“…Yang et al., 2010), while protein phosphatases PP1, PP2A, and calcineurin (CaN) (also known as PP2B) dephosphorylate GluA1 S845 and remove receptors by endocytosis during LTD (Mulkey et al., 1993; Kameyama et al., 1998; Lee et al., 1998, 2000, 2003, 2010; Beattie et al., 2000; Ashby et al., 2004).”
BackgroundMechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus
Mulkey, R. M., & Malenka, R. C. (1992) · Neuron · doi:10.1016/0896-6273(92)90248-c · Cited by 1,113 · cited 2×
“AKAP150-anchored CaN is required for LTD Previous studies found LTD impairments at CA1 synapses in forebrain-restricted, conditional CaN knock-out mice and inhibition of LTD by CaN phosphatase inhibitors using a standard low-frequency stimulation (LFS) LTD induction protocol (900 pulses at 1 Hz) (Dudek and Bear, 1992;…”
MethodReinsertion or Degradation of AMPA Receptors Determined by Activity-Dependent Endocytic Sorting
Ehlers, M. D. (2000) · Neuron · doi:10.1016/s0896-6273(00)00129-x · Cited by 1,096 · cited 3×
“…protein kinase (PKA) increases channel open probability and promotes receptor recycling and exocytosis at extrasynaptic sites near the postsynaptic density (PSD) (Banke et al., 2000; Ehlers, 2000; Esteban et al., 2003; Oh et al., 2006; Man et al., 2007; Yang et al., 2008; He et al., 2009).”
BackgroundInvolvement of a calcineurin/ inhibitor-1 phosphatase cascade in hippocampal long-term depression
Mulkey, R. M., Endo, S., Shenolikar, S., & Malenka, R. C. (1994) · Nature · doi:10.1038/369486a0 · Cited by 1,083 · cited 2×
“AKAP150-anchored CaN is required for LTD Previous studies found LTD impairments at CA1 synapses in forebrain-restricted, conditional CaN knock-out mice and inhibition of LTD by CaN phosphatase inhibitors using a standard low-frequency stimulation (LFS) LTD induction protocol (900 pulses at 1 Hz) (Dudek and Bear, 1992;…”
MethodAMPAR Removal Underlies Aβ-Induced Synaptic Depression and Dendritic Spine Loss
Hsieh, H., Boehm, J., Sato, C., Iwatsubo, T., Tomita, T., Sisodia, S., & Malinow, R. (2006) · Neuron · doi:10.1016/j.neuron.2006.10.035 · Cited by 1,042
PKA phosphorylation of AMPA receptor subunits controls synaptic trafficking underlying plasticity
Esteban, J. A., Shi, S.-H., Wilson, C., Nuriya, M., Huganir, R. L., & Malinow, R. (2003) · Nature Neuroscience · doi:10.1038/nn997 · Cited by 894 · cited 2×
“Importantly, forms of LTP that are regulated by PKA also involve GluA2-lacking receptors and S845 phosphorylation (Esteban et al., 2003; Lee et al., 2003, 2010; Lu et al., 2007; Yang et al., 2010; Qian et al., 2012).”
BackgroundLee, H.-K., Takamiya, K., Han, J.-S., Man, H., Kim, C.-H., Rumbaugh, G., Yu, S., Ding, L., He, C., Petralia, R. S., et al. (2003) · Cell · doi:10.1016/s0092-8674(03)00122-3 · Cited by 802 · cited 4×
“Using a stronger LTD induction protocol that delivers a 1 Hz paired pulse with a 50 ms interpulse interval, which was also shown to be NMDAR dependent in mice (Lee et al., 2003), LTD was still strongly impaired in PIX compared with WT slices [Fig.”
BackgroundResultInfluentialRegulation of AMPA receptor endocytosis by a signaling mechanism shared with LTD
Beattie, E. C., Carroll, R. C., Yu, X., Morishita, W., Yasuda, H., von Zastrow, M., & Malenka, R. C. (2000) · Nature Neuroscience · doi:10.1038/81823 · Cited by 745
Cited by
Sorted by citations
Items 101–137 of 137
Simmons, S. C., Flerlage, W. J., Langlois, L. D., Shepard, R. D., Bouslog, C., Thomas, E. H., Gouty, K. M., Sanderson, J. L., Gouty, S., Cox, B. M., et al. (2024) · Communications Biology · doi:10.1038/s42003-024-06041-8 · Cited by 11
Self-citationLameth, J., Arnaud‐Cormos, D., Lévêque, P., Boillée, S., Edeline, J., & Mallat, M. (2020) · Neurotoxicity Research · doi:10.1007/s12640-020-00191-3 · Cited by 9
Itakura, M., Watanabe, I., Sugaya, T., & Takahashi, M. (2014) · FEBS Journal · doi:10.1111/febs.12708 · Cited by 10
Proteasomal-Mediated Degradation of AKAP150 Accompanies AMPAR Endocytosis during cLTD
Cheng, W., Siedlecki‐Wullich, D., Català-Solsona, J., Fábregas, C., Fadó, R., Casals, N., Solé, M., Unzeta, M., Saura, C. A., Rodrı́guez-Álvarez, J., et al. (2020) · eNeuro · doi:10.1523/eneuro.0218-19.2020 · Cited by 10
“A-kinase anchoring protein 79 (AKAP79; in human) or AKAP150 (the rodent homolog) is a postsynaptic scaffold protein that anchors PKA, PKC, and CaN to the PSD, regulating AMPAR phosphorylation, trafficking and activity associated with LTP and LTD (Tavalin et al., 2002; Smith et al., 2006; Lu et al., 2007, 2008; Tavalin…”
BackgroundInfluentialGlutamate treatment mimics LTP- and LTD-like biochemical activity in viable synaptosome preparation
Gharami, K., & Biswas, S. C. (2019) · Neurochemistry International · doi:10.1016/j.neuint.2019.104655 · Cited by 9
Zhou, J., Shao, J., Chen, S., Chen, H., & Pan, H. (2024) · The Journal of Physiology · doi:10.1113/jp286081 · Cited by 10
“Phosphorylation plays a critical role in the dynamic regulation of synaptic AMPAR composition (Sanderson et al., 2012).”
BackgroundWang, S., Xia, Z., Yang, S., Chen, W., Zhao, Y., Li, M., Tian, D., Pan, Y., Lin, X., Zhu, X., et al. (2024) · British Journal of Pharmacology · doi:10.1111/bph.16318 · Cited by 9
“Furthermore, we also examined the action of Ht-31 on GluA1 in the BLA after CRS, and as the results showed, CRS raised the surface expression and Ser-845 phosphorylation level of GluA1, which was also reversed by Ht-31 incubation (Figure 3f,g).”
BackgroundInfluentialBiophysics of Voltage-Gated Ion Channels
Lipscombe, D., & Toro, C. P. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-397179-1.00013-0 · Cited by 7
Midorikawa, R., Wakazono, Y., & Takamiya, K. (2024) · Journal of Cell Science · doi:10.1242/jcs.261281 · Cited by 6
The evolution of AKAPs and emergence of PKA isotype selective anchoring determinants
Falcone, J. I., Cleveland, K. H., Kang, M., Odle, B. J., Forbush, K. A., & Scott, J. D. (2025) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2025.108480 · Cited by 7
“These regulatory subunits are enriched in the central nervous system and organize complex behaviors such as excitatory synaptic transmission and molecular elements of learning and memory (60, 85, 86).”
Protein Phosphatase 2B Dual Function Facilitates Synaptic Integrity and Motor Learning
Lin, Z., Wu, B., Paul, M. W., Li, K. W., Yao, Y., Smal, I., Onori, M. P., Hasanbegović, H., Bezstarosti, K., Demmers, J., et al. (2021) · Journal of Neuroscience · doi:10.1523/jneurosci.1741-20.2021 · Cited by 6
“In hippocampal pyramidal cells, PP2B directly dephosphorylates Ser845 of the AMPA-type GluR1 subunit (Jurado et al., 2010; Sanderson et al., 2012), which in turn regulates receptor insertion and removal from the membrane, underlying induction of LTP and LTD, respectively (Roche et al., 1996).”
BackgroundCararo-Lopes, M. M., de Souza, D. G., Ganzella, M., Hansel, G., Kazlauckas, V., Mello, P. S. D., Lima, L. D. S., Kawamoto, E. M., Portela, L. V., Souza, D. O., et al. (2022) · Journal of Affective Disorders Reports · doi:10.1016/j.jadr.2022.100394 · Cited by 6
Gibson, E. S., Woolfrey, K. M., Li, H.-M., Hogan, P., Nemenoff, R., Heasley, L., & Dell'Acqua, M. (2018) · Molecular Pharmacology · doi:10.1124/mol.118.113159 · Cited by 5
“20 at A SPE T Journals on A pril 9, 2022 m olpharm .aspetjournals.org nloaded from Sanderson et al., 2012; Grigoriu et al., 2013; Murphy et al., 2014).”
BackgroundSelf-citationChu, C.-C., Hu, Y.-H., Li, G.-Z., Chen, J., Zhang, N.-N., Gu, Y., Wu, S., Zhang, H., Xu, Y.-Y., Guo, H.-L., et al. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.106812 · Cited by 4
“This regulation involves the phosphorylation of GluA1 at serine 845 (Ser845) during long-term potentiation (LTP) and LTD (Hell, 2016; Purkey and Dell ’ Acqua, 2020; Sanderson et al., 2016; Sanderson et al., 2012; Sanderson et al., 2018; Smith et al., 2006).”
Combs‐Bachmann, R. E., Johnson, J., Vytla, D., Hussey, A. M., Kilfoil, M., & Chambers, J. J. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13051 · Cited by 4
Huang, Y., (邵建英), J.-Y. S., Chen, H., Zhou, J., Chen, S.-R., & Pan, H. (2024) · Journal of Neuroscience · doi:10.1523/jneurosci.0392-24.2024 · Cited by 3
Role of calcineurin and ionotropic glutamate receptors in Alzheimer's disease: A systematic review
Teklemariam, A. B., Zewde, E. A., Agidew, M. M., Siyamrew, S. A., Maru, L., & Muche, Z. T. (2025) · Brain Disorders · doi:10.1016/j.dscb.2025.100218 · Cited by 3
Guo, Q. (2024) · Neuroscience Research · doi:10.1016/j.neures.2024.10.003 · Cited by 2
Speca, D. J., He, C.-W., Meyer, C. M., Scott, E. C., & Díaz, E. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1526034 · Cited by 3
Hypothetical gene C18orf42 encodes a novel protein kinase A‐binding protein
Fukuda, M., & Aizawa, Y. (2015) · Genes to Cells · doi:10.1111/gtc.12217 · Cited by 2
“To test this, we characterized complex formation of the RIIa subunit with three different AKAP members that are functional in neural PKA signaling (AKAP1, AKAP5 and MAP2; Dickey & Strack 2011; Sanderson et al. 2012; Huang et al. 2013) by pull-down assay (Fig.”
BackgroundMethodInfluentialDHHC2-Mediated AKAP150 Palmitoylation Regulates Hippocampal Synaptic Plasticity and Fear MemoryPreprint
Li, M., Huang, D.-H., Zheng, Y., Tian, D., Ouyang, H. X., Song, K.-X., Huang, Z., Lin, X., Zhu, X.-Q., Huang, J., et al. (2022) · Research Square · doi:10.21203/rs.3.rs-2180782/v1 · Cited by 2
Zhang, S., Jeon, Y.-J., Han, J., Park, H.-Y., & Chung, C. (2025) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2025.102801 · Cited by 1
Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity
Feighan, K. M., Thakare, H. K., Glasgow, S. D., & Kennedy, T. E. (2026) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2026.1761008 · Cited by 2
“Moreover, S845 is required for synaptic upscaling, as both a phospho-deficient knockin mutation (S845A) and knockout of A-kinase anchor protein 5 (AKAP5), the scaffolding protein that links PKA (and calcineurin) with GluA1, is sufficient to block TTX-mediated increases in excitatory synaptic activity (Diering et al.,…”
InfluentialMilner, T. A., Sommer, G., Wang, G., jaouni, N., Hussein, S. O., & Glass, M. J. (2026) · Biology of Sex Differences · doi:10.1186/s13293-026-00922-9 · Cited by 1
“Given that AKAP150 couples AMPA GluA1 receptors to presumably functional sites on the plasma membrane [56, 57], the subcellular location of AKAP150-SIG particles may provide some functionally important information.”
Investigation Of The Molecular Mechanisms Of Synaptic Tagging And Capture
Park, J. W. (2014) · Scholarly Commons (University of Pennsylvania) · Cited by 1
Targeting AKAP79/150 in Human Disorders: An Emerging Opportunity for Future Therapies?
Chen, F., Chu, C.-C., Wu, C., Chen, F., Xu, J., Zhou, L., Fang, W. R., Lu, X., & Hu, Y. H. (2023) · Progress in Neurobiology · doi:10.60124/j.pneuro.2023.10.06
Csmd2 interacts with Dab1 and is Required in Reelin-Mediated Neuronal MaturationPreprint
Gutierrez, M. A., Dwyer, B. E., & Franco, S. J. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.01.30.925537 · Cited by 1
“Synaptosomal Fractionation Preparation of crude synaptosomal fractions and crude postsynaptic density fractions were prepared from mouse forebrain homogenate was performed as previously described (Sanderson et al., 2012).”
MethodSimmons, S. C., Flerlage, W. J., Langlois, L. D., Shepard, R. D., Bouslog, C., Thomas, E. H., Gouty, K. M., Sanderson, J. L., Gouty, S., Cox, B. M., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.12.06.570160 · Cited by 1
Self-citationDennison, C. L. (2014) · White Rose eTheses Online (University of Leeds, The University of Sheffield, University of York)
Protein Interactions Regulate KCC2-mediated Chloride Homeostasis
Pressey, J. C. (2015) · TSpace (University of Toronto)
CaMKII binding to GluN2B flips a β-adrenergic switch from synaptic depression to potentiationPreprint
Buonarati, O. R., Larsen, M. E., Qian, H., Hell, J. W., & Bayer, K. U. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.06.23.497296
“…somewhat controversial (Gray et al., 2016), as others have found block of LTD not only by glutamate-competitive inhibitors, but also by the pore blocker MK801 (Babiec et al., 2014; Coultrap et al., 2014; Dudek and Bear, 1992; Massey et al., 2004; Mulkey and Malenka, 1992; Sanderson et al., 2012).”
BackgroundSex differences in AMPA receptor trafficking proteins
Roberts, M. Y., & Briand, L. A. (2026) · Biology of Sex Differences · doi:10.1186/s13293-026-00849-1
“When calcineurin anchoring to AKAP79/150 is disrupted, phosphorylation of S845 increases and removal of GluA1 from the synapse is impaired [100, 101].”
Pathophysiological consequences of a Fragile X missense mutation
Garcia, M. P. (2020) · theses.fr (ABES) · doi:10.70675/b8e86263z5926z4a83zbaf6z0f61bf2d15f9
Ruan, M., Ma, S., Wang, X., Zhang, F., & Zhang, H. (2026) · Neuropharmacology · doi:10.1016/j.neuropharm.2026.110968
Anchored kinase and phosphatase signaling networks in amyloid β-induced synaptic dysfunction
Koek, L. A., Jo, H.-N., Kennedy, M. J., & Dell’Acqua, M. L. (2026) · Molecular Pharmacology · doi:10.1016/j.molpha.2026.100141
Self-citationCALCINEURIN-MEDIATED SIGNALING IN ISCHEMIC PRECONDITIONING AND NEURONAL CELL DEATH
Shah, N. H. (2014) · D-Scholarship@Pitt (University of Pittsburgh)
Metadata
- Authors
- Sanderson, J. L., Gorski, J. A., Gibson, E. S., Lam, P., Freund, R. K., Chick, W. S., & Dell'Acqua, M. L.
- Affiliations
- University of Colorado Anschutz (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-10-24
- Volume
- 32
- Issue
- 43
- Pages
- 15036-15052
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3504485
- OpenAlex
- W1998026266
- Cited by
- 137
- References
- 76
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 11 · 2023: 8 · 2022: 6 · 2021: 11 · 2020: 10 · 2019: 6 · 2018: 7 · 2017: 9 · 2016: 13 · 2015: 21 · 2014: 15 · 2013: 8 · 2012: 1
- FWCI
- 5.41
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (submittedVersion)
- PubMed Central (submittedVersion)
- Funders
- American Heart Association
- National Institutes of Health (T32AA007464, UL1 RR025780, P30NS048154, NS040701)
- Anschutz Medical Campus, University of Colorado (P30 NS048154)
- National Institute on Alcohol Abuse and Alcoholism (T32AA007464)
- National Institute of Neurological Disorders and Stroke (P30NS-048154, NS040701, R01NS040701)
- National Center for Research Resources (#UL1 RR025780)
- Colorado Clinical and Translational Sciences Institute (UL1-RR025780)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- AKAP150, calcineurin, AMPA receptors, GluR1, GluA2, synaptic plasticity, long-term potentiation, long-term depression, protein kinase A, extrasynaptic receptors, PSD-95, Ca2+-permeable AMPA receptors, hippocampus
- MeSH terms
- Disks Large Homolog 4 Protein, Action Potentials, Analysis of Variance, Animals, Biophysics, Calcium, Cells, Cultured, Electric Stimulation, Female, Hippocampus, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Neuronal Plasticity, Neurons, Phosphorylation, Quinoxalines, Serine, Subcellular Fractions, Synapses, Tetrodotoxin, N-Methylaspartate, Silver Staining, Receptors, AMPA, Patch-Clamp Techniques, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Calcineurin, Excitatory Postsynaptic Potentials, Sodium Channel Blockers, Immunoprecipitation, Dendritic Spines, Mice, Guanylate Kinases, A Kinase Anchor Proteins, In Vitro Techniques
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