The DOI matches its Crossref record; 95 of the 99 references it cites were found in a registry or an index; 19 of the 124 sources its claims cite were checked for support.
NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD).
Open accessAbstract
Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-d-aspartate (NMDA)-type glutamate receptors, typically by the coincident activity of pre- and postsynaptic neurons. The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses. With time, structural changes become apparent, which in general require the synthesis of new proteins. The investigation of the molecular and cellular mechanisms underlying these forms of synaptic plasticity has received much attention, because NMDA receptor-dependent LTP and LTD may constitute cellular substrates of learning and memory.
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Claims the paper makes
40 No full text of the sources · 27 Sources not found · 24 Own interpretation · 17 No basis given · 7 Partly supported · 5 Supported · 5 Supported so far · 5 Not checked yet · 1 Not supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The insertion and removal of AMPARs during LTP and LTD, respectively, is believed to involve classical mechanisms of SNARE protein -mediated exocytosis and dynamin-dependent endocytosis via clathrin-coated vesicles (Lu ¨scher et al. 1999;Carroll et al. 2001;Kennedy and Ehlers 2011).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
- Not matchedcites Lu ¨scher et al. 1999
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Carroll et al. 2001 source
- Partly supportedcites Kennedy and Ehlers 2011 sourceExperimental — accuracy not yet measured
The section “Postsynaptic Exocytosis and Synaptic Plasticity” describes SNARE-mediated postsynaptic fusion as a mechanism implicated in AMPA-receptor insertion during LTP. Our copy does not substantiate the other half of the claim: AMPA-receptor removal during LTD by dynamin-dependent endocytosis through clathrin-coated vesicles. (LLM, conf=0.88)
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.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This leads to the phosphorylation of a number of proteins including AMPARs themselves (Derkach et al. 1999).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
What the sources say
- Partly supportedcites Derkach et al. 1999 sourceExperimental — accuracy not yet measured
The Results report that activated CaMKII greatly enhances phosphorylation of the AMPAR subunit GluR1 at Ser-831, and the Discussion identifies CaMKII-mediated phosphorylation of AMPARs. These passages support the AMPAR part of the claim, but do not establish that CaMKII phosphorylates a number of other proteins. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, interactions between neighboring synapses do occur, such that the intradendritic spread of the activated Ras from an active synapse briefly lowers the threshold for subsequent LTP induction at neighboring synapses (Harvey et al. 2008).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Supportedcites Harvey et al. 2008 source
The Abstract (p. 1) reports that Ras activity diffuses from an LTP-stimulated spine into nearby spines, decays in approximately five minutes, and is necessary for local regulation of the LTP-induction threshold. The synaptic crosstalk experiment (p. 3) shows that a protocol too weak to induce plasticity alone becomes sufficient at a neighboring spine after LTP at the first spine. (LLM, conf=0.94)
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 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
“Experiments using this approach to induce NMDAR-dependent LTP have shown that LTP can be induced at a single synapse without causing postsynaptic potentiation or depression of neighboring synapses (Matsuzaki et al. 2004;Harvey and Svoboda 2007; but see Engert and Bonhoeffer 1997).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Not checked yetcites Matsuzaki et al. 2004 source
Checked before — its earlier verdict is held back until a new check runs.
- Supportedcites Harvey and Svoboda 2007 source
The passage on the LTP protocol (Fig. 1a–b; page not supplied) reports lasting potentiation at the stimulated spine but no significant change in uEPSC amplitude or volume at nearby spines. The paper also finds that LTP lowers the threshold for potentiation at a neighboring spine if that spine subsequently receives a subthreshold stimulus; it does not report spontaneous potentiation or depression of unstimulated neighbors. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Engert and Bonhoeffer 1997 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not checked yet
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Heteromeric GluA1/GluA2 receptors seem to be the primary subtype of AMPAR that is inserted into synapses during LTP (Adesnik and Nicoll 2007).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
- Partly supportedcites Adesnik and Nicoll 2007 sourceExperimental — accuracy not yet measured
The Discussion concludes that LTP in CA1 does not involve insertion of calcium-permeable AMPARs, supporting a role for GluA2-containing receptors. But the paper does not identify the inserted receptors specifically as GluA1/GluA2 heteromers or establish that they are the primary subtype across synapses generally. (LLM, conf=0.87)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The underlying molecular mechanisms of I-LTP and I-LTD are variable, but one common feature is that they are often heterosynaptic.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Supportedcites Castillo et al. 2011 source
The Introduction describes different forms of I-LTP and I-LTD with distinct cellular mechanisms. The Presynaptic NMDAR-dependent I-LTD/I-LTP section explicitly refers to their differing underlying molecular mechanisms, supporting the attributed claim. (LLM, conf=0.91)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The underlying molecular mechanisms of I-LTP and I-LTD are variable, but one common feature is that they are often heterosynaptic.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Supportedcites Castillo et al. 2011 source
The section on presynaptic forms of inhibitory synaptic plasticity says that, as in most cases of GABAergic plasticity, their induction is heterosynaptic. Its NMDAR-dependent I-LTD/I-LTP subsection explicitly describes all presynaptic forms of I-LTP and I-LTD as heterosynaptic regardless of molecular mechanism. Page numbers are unavailable in our copy. (LLM, conf=0.93)
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.
- 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
“Insertion of additional receptors therefore is likely to affect the ultrastructure of the synapse, and in fact, spines associated with synapses that underwent LTP enlarge (Matsuzaki et al. 2004;Harvey and Svoboda 2007;Holtmaat and Svoboda 2009;Kasai et al. 2010).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > MAINTENANCE OF LTP AND LTD
What the sources say
- Supportedcites Matsuzaki et al. 2004 source
The passage labeled Abstract describing Figure 4 reports that LTP at small spines was strongly correlated with enlargement of the same spine head. It also says LTP occurred in four of five spines with long-lasting enlargement and in none of four without it. (LLM, conf=0.94)
- Supportedcites Harvey and Svoboda 2007 source
The passage labeled Abstract reports that the LTP protocol produced a long-lasting increase in spine volume at the stimulated spine (Δvol = 78 ± 10%). It also describes spine enlargement as a structural correlate of LTP. This supports the attributed claim; the cited passage does not establish the sentence’s separate suggestion that receptor insertion causes the enlargement. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Holtmaat and Svoboda 2009 source
plaincorrelational- 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.
- 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
“The cognitive decline, however, starts well before this stage, and there is growing evidence that one of the toxic protein species believed to be etiologically related to AD, soluble Ab oligomers, causes early memory problems by disrupting LTP and LTD mechanisms (Walsh et al. 2002;Tanzi 2005;Shankar et al. 2008;Cisse et al. 2011).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SYNAPTIC PLASTICITY AND DISEASE
What the sources say
- Not checked — no full text of the sourcecites Walsh et al. 2002 source
- Not checked — no full text of the sourcecites Tanzi 2005 source
- Supportedcites Shankar et al. 2008 source
The Abstract reports that soluble Aβ oligomers from Alzheimer’s brains inhibit hippocampal LTP, enhance LTD, and disrupt memory of a learned behavior in normal rodents. It also describes altered synapse function as an initial effect, supporting the citing sentence’s broad account of the evidence. (LLM, conf=0.88)
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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Although the vast majority of work on the mechanisms and functions of LTP and LTD have focused on excitatory synapses, potentiation and depression of inhibitory transmission (I-LTP/I-LTD) can also be observed in the brain (Castillo et al. 2011).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Supportedcites Castillo et al. 2011 source
The Introduction identifies long-term potentiation and depression of inhibitory transmission as I-LTP and I-LTD. The nitric oxide-mediated I-LTP section also reports that both potentiation and depression of inhibitory synapses can be induced in the VTA, directly supporting the attributed claim. (LLM, conf=0.95)
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.
- Supported
- It may state two separate claims as one. 41
- Probably not a substantial claim. 6
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
“Consistent with this idea, the spine density increases following LTP induction, and a significantly higher frequency of multiple-spine synapses (Toni et al. 1999) is observed, as well as a reduction of their turnover (De Roo et al. 2008).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > MAINTENANCE OF LTP AND LTD
What the sources say
- Not checked — no full text of the sourcecites Toni et al. 1999 source
- Disputedcites De Roo et al. 2008 sourceExperimental — accuracy not yet measured
The De Roo citation is attached to the claimed reduction in turnover. The Results section, “LTP Induction Results in a Lasting Increase in Protrusion Turnover” (page unavailable), reports that turnover increased for several days after LTP induction; the Discussion likewise calls it a lasting, enhanced turnover. The paper does report selective stabilization of stimulated spines, but not an overall reduction in turnover. (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.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Consistent with original ideas (Bienenstock et al. 1982), modest depolarization can elicit LTD, whereas stronger depolarization leads to LTP.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Partly supportedcites Bienenstock et al. 1982 sourceExperimental — accuracy not yet measured
Section II, “Modification of Cortical Synapses” (page unavailable), proposes that synaptic strength decreases when postsynaptic output is below a modification threshold and increases when it is above it. This supports the claim’s low-versus-high activity pattern, but the paper describes a theoretical rule based on postsynaptic response, not a finding that modest versus stronger depolarization elicits LTD and LTP. (LLM, conf=0.85)
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
“Because the driving force for calcium entry is very large for a neuron at rest and the block of NMDARs by Mg 2þ is incomplete even at resting potentials (Jahr and Stevens 1993), significant Ca enters the cell in response to synaptic stimulation (Sabatini et al. 2002;Bloodgood and Sabatini 2007;Bloodgood et al. 2009) during low-frequency synaptic stimulation.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Partly supportedcites Jahr and Stevens 1993 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites Sabatini et al. 2002 source
- Not checked — no full text of the sourcecites Bloodgood and Sabatini 2007 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These early drug-evoked changes in the properties of excitatory synapses on dopamine cells can be very long-lasting and are followed by many additional synaptic modifications in related structures.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SYNAPTIC PLASTICITY AND DISEASE
What the sources say
- Not checked — no full text of the sourcecites Thomas and Malenka 2003 source
- Not checked — no full text of the sourcecites Kauer and Malenka 2007 source
- Partly supportedcites Wolf and Ferrario 2010 sourceExperimental — accuracy not yet measured
Section 5.3 (page unavailable) reports that early plasticity in VTA dopamine neurons is required for subsequent changes in nucleus accumbens AMPAR transmission, and discusses later adaptations in other VTA targets. It does not establish that the early synaptic changes themselves are very long-lasting; the changes it says persist after long withdrawal are in the nucleus accumbens. (LLM, conf=0.85)
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
“Through this mechanism NMDARs play the role of molecular coincidence detectors, which, as we will see below, is essential for several forms of synaptic plasticity.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > AMPA-TYPE AND NMDA-TYPE GLUTAMATE RECEPTORS
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 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
“The workhorse of glutamatergic transmission is the AMPAR, which drives large and rapid synaptic signaling (Fig. 2).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > AMPA-TYPE AND NMDA-TYPE GLUTAMATE RECEPTORS
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.
In the paper
“Both are ionotropic receptors that are permeable to Na þ and K þ .”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > AMPA-TYPE AND NMDA-TYPE GLUTAMATE RECEPTORS
What the sources say
- Not checked — no full text of the sourcecites Dingledine et al. 1999 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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
“At these CA3-CA1 Schaffer collateral synapses, the loci of both induction and expression are situated in the postsynaptic neuron.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > Abstract
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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses.”
- Also stated in: § EXPRESSION MECHANISM · boosted
“A large body of experimental evidence now supports this hypothesis (Lu ¨scher et al. 2000;Lu ¨scher and Frerking 2001;Malinow and Malenka 2002;Nicoll 2003;Collingridge et al. 2004;Malenka and Bear 2004).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > Abstract
What the sources say
- Not checked — no full text of the sourcecites Lledo et al. 1998 source
- Not matchedcites Lu ¨scher et al. 1999
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- 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.
- Also stated in: § EXPRESSION MECHANISM · boosted
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
“Activation of ionotropic glutamate receptors leads to strong influx of Na þ and only a small efflux of K þ , such that the net effect is the depolarization of the postsynaptic neuron.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > AMPA-TYPE AND NMDA-TYPE GLUTAMATE RECEPTORS
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
“Some of these proteins modulate glutamate receptor function, whereas others control their membrane insertion and removal.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > AMPA-TYPE AND NMDA-TYPE GLUTAMATE RECEPTORS
What the sources say
- Not checked — no full text of the sourcecites Elias and Nicoll 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.
In the paper
“For LTP there is strong evidence that the opening of NMDARs increases calcium concentration sufficiently in the dendritic spine to activate calcium/calmodulin-dependent kinase II (CaMKII), which is found at very high concentrations in spines and which is clearly required for LTP (Lisman et al. 2002).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
What the sources say
- Not checked — no full text of the sourcecites Lisman et al. 2002 source
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.
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
“Because the latter have a higher conductance, this will potentiate the synapse even if the total number remains the same.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
plaindirect- Asserted: fails — The authors may not 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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
“However, this makes sense because high-frequency stimulation protocols cause a strong temporal summation of the excitatory postsynaptic potentials (EPSPs), and the resultant large depolarization of the postsynaptic cell is sufficient to relieve the Mg block of the NMDAR and allow a large amount of calcium to enter the postsynaptic cells during the induction protocol.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
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
“Indeed, it is now fairly well accepted that modest activation of NMDARs leading to modest increases in postsynaptic calcium are optimal for triggering LTD, whereas much stronger activation of NMDARs leading to much larger increases in postsynaptic calcium are required to trigger LTP (Malenka 1994).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Not checked — no full text of the sourcecites Malenka 1994 source
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.
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
“From the perspective of the postsynaptic neuron (which is where the recordings are made), these manipulations lead to both a synaptic potential and an action potential that backpropagates into the dendrites, which presumably provides the additional depolarization required to facilitate calcium influx through the activated NMDARs (Stuart et al. 1997;Waters et al. 2005).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
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.
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
“For LTP induction both pre-and postsynaptic neurons need to be active at the same time because the postsynaptic neuron must be depolarized when glutamate is released from the presynaptic bouton to fully relieve the Mg 2þ block of NMDARs.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
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
“These ubiquitous forms of short-term synaptic plasticity are greatly influenced by the baseline release probability yet were unaffected by the generation of LTP (McNaughton 1982;Manabe et al. 1993; but see Schulz et al. 1995).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
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.
In the paper
“NMDAR-dependent LTP is therefore an associative form of plasticity and fulfills the criteria for correlated activity as the origin of the strengthening of the connection between two neurons proposed by Donald Hebb more than 60 years ago (Hebb 1949).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
- Not matchedcites Hebb 1949
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
None of the sources cited for this claim have been checked yet.
In the paper
“There is, however, no change in the size of these currents after induction of LTP even though other manipulations that affect transmitter release have clear effects.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
- Not checked — no full text of the sourcecites Diamond et al. 1998 source
- Not matchedcites Lu ¨scher et al. 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Of particular interest are members of the TARP family, which interact with all AMPA receptor subunits and control not only membrane insertion but also lateral redistribution (Chen et al. 2000;Tomita et al. 2005; see Blakely and Edwards 2012).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As a consequence of coincident depolarization and glutamate binding, calcium influx through NMDARs is maximal, which activates intracellular signaling cascades that ultimately are responsible for the altered synaptic efficacy.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
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
“As the direction of synaptic plasticity depends on the timing between the presynaptic and postsynaptic spikes, this phenomenon has been named spike-timing-dependent plasticity (Dan and Poo 2006;Caporale and Dan 2008).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: 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
“This causes only a modest amount of postsynaptic depolarization, resulting in a modest but prolonged increase in postsynaptic calcium due to modest and repetitive activation of NMDARs.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
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
“Appropriate coincident activity of the pre-and postsynaptic neurons causes an influx of calcium through NMDARs, and depending on the quantitative characteristics of this calcium signal, AMPARs are either inserted into or removed from the synapses, resulting in LTP or LTD, respectively.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
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
“Importantly, it was found that the rate of this decrease remains unaltered by LTP but is clearly affected by other manipulations that are known to influence the probability of transmitter release (Manabe and Nicoll 1994).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
- Not checked — no full text of the sourcecites Manabe and Nicoll 1994 source
boosted- 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
“This result immediately raised the possibility that at both silent synapses and synapses that already contain AMPARs, LTP involves the insertion of more AMPARs into the synapse, whereas conversely, LTD may involve the removal or endocytosis of synaptic AMPARs (Fig. 3) (Lledo et al. 1998;Lu ¨scher et al. 1999).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > EXPRESSION MECHANISM
What the sources say
- Not checked — no full text of the sourcecites Lledo et al. 1998 source
- Not matchedcites Lu ¨scher et al. 1999
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- 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
“Furthermore, the toxic Ab also decreases synaptic NMDARs, a change that contributes to the impaired LTP (Kamenetz et al. 2003).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SYNAPTIC PLASTICITY AND DISEASE
What the sources say
- Not checked — no full text of the sourcecites Kamenetz et al. 2003 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It is induced by activation of NMDARs (and sometimes voltagegated calcium channels) and modulated by GABA B receptors, which together drive an increase in cytoplasmic calcium, in part by triggering the release of calcium from intracellular stores.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Not checked — no full text of the sourcecites Inagaki et al. 2008 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.
In the paper
“Such perforated synapses also contain a higher proportion of smooth endoplasmic reticulum and a spine apparatus (Lu ¨scher et al. 2000).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > MAINTENANCE OF LTP AND LTD
What the sources say
- Not matchedcites Lu ¨scher et al. 2000
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
It may state two separate claims as one.
- Not matched
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
“Importantly, this manipulation occludes further LTP, suggesting a shared mechanism between the ways of increasing synaptic strength (Malenka and Nicoll 1999;Lisman et al. 2002).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
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.
In the paper
“The increase of this IPSP also depends on NMDAR activation and CaMKII, thus sharing two key properties with hippocampal LTP of AMPARs.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Not checked — no full text of the sourcecites Huang et al. 2005 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This is a very attractive model because calcineurin has a much higher affinity for calcium/calmodulin than does CaMKII and thus will be preferentially activated by a modest increase in calcium, the exact trigger for LTD.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
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.
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
“Synaptic plasticity of GABAergic transmission needs the activation of glutamatergic synapses and a specific messenger that passes the signal from one type of synapses to the other.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
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 this model NMDAR activation leads to postsynaptic release of BDNF, which functions as a retrograde messenger and causes an increase in GABA release through activation of presynaptic TrkB receptors.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Not checked — no full text of the sourcecites Inagaki et al. 2008 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.
In the paper
“Indeed, a very influential model proposed that NMDAR-dependent LTD depends on the calcium/calmodulin-dependent protein phosphatase calcineurin as well as on protein phosphatase 1 (PP1) (Lisman 1989).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SIGNALING CASCADES FOR TRIGGERING LTP AND LTD
What the sources say
- Not checked — no full text of the sourcecites Lisman 1989 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This leads to activation of a Ca 2þ -dependent nitric oxide synthase, which generates nitric oxide, which acts as a retrograde messenger by diffusing back to presynaptic neurons.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > NMDAR-DEPENDENT LTP OF INHIBITORY TRANSMISSION
What the sources say
- Not checked — no full text of the sourcecites Nugent 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.
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
“Through these mechanisms LTP may guide the selective stabilization of synaptic inputs that show coincident activity, whereas nonactivated inputs may be removed and replaced by new spines.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > MAINTENANCE OF LTP AND LTD
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Direct application or overproduction of Ab oligomers both inhibits LTP and triggers LTD-like changes (Fig. 5).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SYNAPTIC PLASTICITY AND DISEASE
What the sources say
- Not matchedcites Fig. 5
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
In the paper
“Soluble Ab oligomers strongly activate metabotropic glutamate receptors (mGluRs), which leads to the internalization of AMPARs and LTD.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > CONCLUSIONS
What the sources say
- Not matchedcites Fig. 5
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- 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
In the paper
“This drug-evoked plasticity requires activation of type 1 dopamine receptors along with NMDAR activation and is expressed by a redistribution of AMPARs and NMDARs.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > SYNAPTIC PLASTICITY AND DISEASE
What the sources say
- Not checked — no full text of the sourcecites Ungless et al. 2001 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.
In the paper
“In a second step synapses become thinner and some disappear.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > CONCLUSIONS
What the sources say
- Not matchedcites Fig. 5
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
In the paper
“AMPA receptors have a linear I -V relationship when they contain the subunit GluA2, but are inward-rectifying (see text for definition) without GluA2.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > CONCLUSIONS
What the sources say
- Not matchedcites Fig. 2
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: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“At the same time they inhibit NMDARs, precluding the induction of LTP.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > CONCLUSIONS
What the sources say
- Not matchedcites Fig. 5
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
The paper relies on this without support.
NMDAR-dependent LTP and LTD are cellular substrates or correlates of learning and memory.
“The investigation of the molecular and cellular mechanisms underlying these forms of synaptic plasticity has received much attention, because NMDA receptor-dependent LTP and LTD may constitute cellular substrates of learning and memory.”
“Because both LTP and LTD are believed to represent cellular correlates of learning and memory, they have attracted considerable interest.”
The paper relies on this without support.
NMDAR-dependent LTP and LTD are triggered in the postsynaptic cell.
“This is re-quired because it is well established that NMDAR-dependent LTP and LTD are triggered in the postsynaptic cell.”
The paper relies on this without support.
Altered LTP and LTD contributes to the pathophysiology of brain diseases such as dementia, movement disorders, depression, addiction, posttraumatic stress syndrome, neuropathic pain, and anxiety disorders.
“Altered LTP and LTD has been implicated as a mechanism that may contribute to brain diseases as diverse as dementia, movement disor-ders, depression, addiction, posttraumatic stress syndrome, neuropathic pain, and anxiety disorders.”
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?
In the citing paper
“The decreased A/N ratios of M1/M2-to-DLS synapses indicate decreased synaptic strength, since typically it is the number of functional AMPAR, not NMDAR, that changes in the synaptic composition when synapses modify their strength [23].”
From Projection-specific deficits in synaptic transmission in adult Sapap3-knockout mice (2020) · cites this paper as [23]
In the citing paper
“The decreased A/N ratios of M1/M2-to-DLS synapses indicate decreased synaptic strength, since typically it is the number of functional AMPAR, not NMDAR, that changes in the synaptic composition when synapses modify their strength [23].”
From Projection-specific deficits in synaptic transmission in adult Sapap3-knockout mice (2020) · cites this paper as [23]
In the citing paper
“the colocalization of schizophrenia-associated SNVs with class 3 loops suggests that defects in enhancer decommissioning might contribute to synaptic plasticity defects in neuropsychiatric diseases47.”
From Three-dimensional genome restructuring across timescales of activity-induced neuronal gene expression (2020) · cites this paper as [47]
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
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > CONCLUSIONS
“Coinci-dent activity in pre-and postsynaptic neurons resulting in calcium influx through synaptic NMDARs is well established to be necessary for the triggering of both LTP and LTD.”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > INDUCTION OF LTP AND LTD
“Conversely, LTD can be induced by repeated activation of the presynaptic neuron at low frequencies without postsynaptic activity (see below).”
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
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > MAINTENANCE OF LTP AND LTD
“Moreover, selective interference with the structural changes that accompany LTD do not seem to affect the increase in synaptic strength, at least not in early stages, up to 1 -2 hr following induction (Fig. 4) (Wang et al. 2007;Redondo and Morris 2011).”
§ NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) > Abstract
“More receptors are added to potentiate the synapse or receptors are removed to weaken synapses.”
Citations
Cites
A synaptic model of memory: long-term potentiation in the hippocampus
Bliss, T. V. P., & Collingridge, G. L. (1993) · Nature · doi:10.1038/361031a0 · Cited by 11,566
The Organization of Behavior; A Neuropsychological Theory.
Attneave, F., B., M., & Hebb, D. O. (1950) · The American Journal of Psychology · doi:10.2307/1418888 · Cited by 5,146
Walsh, D. M., Klyubin, I., Fadeeva, J. V., Cullen, W. K., Anwyl, R., Wolfe, M. S., Rowan, M. J., & Selkoe, D. J. (2002) · Nature · doi:10.1038/416535a · Cited by 4,291
The Organization of Behavior: A Neuropsychological Theory
(1950) · JAMA · doi:10.1001/jama.1950.02910470083028 · Cited by 4,272
Malenka, R. C., & Bear, M. F. (2004) · Neuron · doi:10.1016/j.neuron.2004.09.012 · Cited by 3,968
Self-citationShankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
Glutamate receptor ion channels
Mayer, M. L. (2005) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2005.05.004 · Cited by 3,655
The Glutamate Receptor Ion Channels
Dingledine, R., Borges, K., Bowie, D., & Traynelis, S. F. (1999) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01394-2 · Cited by 3,554
Bienenstock, E., Cooper, L., & Munro, P. (1982) · The Journal of Neuroscience · doi:10.1523/jneurosci.02-01-00032.1982 · Cited by 2,896
Long-Term Potentiation--A Decade of Progress?
Malenka, R. C., & Nicoll, A. R. A. (1999) · Science · doi:10.1126/science.285.5435.1870 · Cited by 2,729
Self-citation
Cited by
Sorted by citations
AMPARs and Synaptic Plasticity: The Last 25 Years
Huganir, R. L., & Nicoll, R. A. (2013) · Neuron · doi:10.1016/j.neuron.2013.10.025 · Cited by 968
“, 2012) and AMPAR trafficking (Anggono and Huganir, 2012; Kessels and Malinow, 2009; Lüscher and Malenka, 2012; Nicoll and Roche, 2013).”
Role of Glutamate and NMDA Receptors in Alzheimer’s Disease
Wang, R., & Reddy, P. H. (2017) · Journal of Alzheimer’s Disease · doi:10.3233/jad-160763 · Cited by 1,009
“On the contrary, a modest activation of NMDARs causes a modest increase in postsynaptic Ca 2 + and triggers phosphatase-mediated long-term depression [15].”
Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988
“As a glutamate receptor, functional NMDARs regulate the formation of synapes and synaptic plasticity.(78) AβOs directly disturb the activity of NMDARs and impair NMDAR-mediated signaling pathways (e.”
BackgroundSynaptic Plasticity Forms and Functions
Magee, J. C., & Grienberger, C. (2020) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-090919-022842 · Cited by 806
“The overlap of these two signals initiates synaptic plasticity expression mechanisms that are perhaps the same as those found for standard LTP (Luscher & Malenka 2012, Kandel et al. 2014).”
BackgroundInfluentialMechanisms of neuronal cell death in ischemic stroke and their therapeutic implications
Tuo, Q., Zhang, S., & Lei, P. (2021) · Medicinal Research Reviews · doi:10.1002/med.21817 · Cited by 771
“Once glutamate binds to NMDARs, Ca channels are opened.(32)”
Background
Metadata
- Authors
- Luscher, C., & Malenka, R. C.
- Affiliations
- Stanford Medicine (US)
- ORCID
- Malenka, R. C.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-04-17
- Volume
- 4
- Issue
- 6
- Pages
- a005710-a005710
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC3367554
- OpenAlex
- W2137841176
- Cited by
- 1,110
- References
- 99
- Citations by year
- 2026: 72 · 2025: 119 · 2024: 128 · 2023: 87 · 2022: 76 · 2021: 107 · 2020: 101 · 2019: 95 · 2018: 98 · 2017: 75 · 2016: 56 · 2015: 37 · 2014: 30 · 2013: 22 · 2012: 5
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- NMDA receptor, long-term potentiation, long-term depression, synaptic plasticity, learning and memory, protein synthesis
- MeSH terms
- Humans, Learning, Memory, Signal Transduction, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Long-Term Synaptic Depression
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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