NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD).

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).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lu ¨scher et al. 1999
• ?Not checked — no full text of the sourcecites Carroll et al. 2001 source
• Partly supported

  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)

  cites Kennedy and Ehlers 2011 sourceExperimental — accuracy not yet measured

In the paper

“This leads to the phosphorylation of a number of proteins including AMPARs themselves (Derkach et al. 1999).”

What the sources say

• Partly supported

  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)

  cites Derkach et al. 1999 sourceExperimental — accuracy not yet measured

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).”

What the sources say

• Supported

  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)

  cites Harvey et al. 2008 source

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).”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites Matsuzaki et al. 2004 source
• Supported

  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)

  cites Harvey and Svoboda 2007 source
• ?Not checked — no full text of the sourcecites Engert and Bonhoeffer 1997 source

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).”

What the sources say

• Partly supported

  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)

  cites Adesnik and Nicoll 2007 sourceExperimental — accuracy not yet measured

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.”

What the sources say

• Supported

  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)

  cites Castillo et al. 2011 source

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.”

What the sources say

• Supported

  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)

  cites Castillo et al. 2011 source

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).”

What the sources say

• Supported

  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)

  cites Matsuzaki et al. 2004 source
• Supported

  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)

  cites Harvey and Svoboda 2007 source
• ?Not checked — no full text of the sourcecites Holtmaat and Svoboda 2009 source

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).”

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
• Supported

  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)

  cites Shankar et al. 2008 source

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).”

What the sources say

• Supported

  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)

  cites Castillo et al. 2011 source

In the paper

“Conversely, the triggering of LTD is associated with the shrinkage of dendritic spines and perhaps even their disappearance (Na ¨gerl et al. 2004;Zhou et al. 2004;Wang et al. 2007;Kasai et al. 2010).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Na ¨gerl et al. 2004
• Supported

  The Results report that low-frequency stimulation inducing LTD was followed by spine shrinkage, with some spines retracting (Figure 1). The Discussion also notes instances of spine-head disappearance (Figures 1D and 1F), while cautioning that the roughly one-hour experiments could not establish whether synapses were ultimately eliminated. The claim’s tentative “perhaps” is consistent with that limit. (LLM, conf=0.91)

  cites Zhou et al. 2004 source
• ?Not checked — no full text of the sourcecites Wang et al. 2007 source

In the paper

“Addictive drugs also have profound effects on synaptic transmission that may influence LTP and LTD (Wolf 2003;Kauer and Malenka 2007;Lu ¨scher and Malenka 2011).”

What the sources say

• ?Not checked — no full text of the sourcecites Wolf 2003 source
• ?Not checked — no full text of the sourcecites Kauer and Malenka 2007 source
• Supported

  The Nucleus accumbens section says drugs of abuse can alter mechanisms that produce LTP and LTD and influence subsequent synaptic plasticity. The section on acute drug effects also says addictive drugs modify synaptic transmission. No page numbers are provided in the supplied copy. (LLM, conf=0.93)

  cites Lüscher and Malenka 2011 source

In the paper

“Arc is one immediate early gene that may orchestrate the translation of dendritic mRNA required for actin polymerization and stable expansion of dendritic spines during LTP (Bramham et al. 2010).”

What the sources say

• Supported

  The Introduction identifies Arc as an immediate early gene whose mRNA is transported to dendrites and translated locally. The Conclusions and future directions describe a working hypothesis linking Arc synthesis, local translation, actin stabilization and stable spine expansion during LTP consolidation; the claim’s “may” preserves that uncertainty. (LLM, conf=0.88)

  cites Bramham et al. 2010 source

In the paper

“For example, in the nucleus accumbens chronic (5-d) administration of cocaine triggers an internalization of AMPARs in medium spiny neurons, a change that occludes the subsequent synaptic induction of NMDARdependent LTD (Thomas and Malenka 2003;Kauer and Malenka 2007;Wolf and Ferrario 2010).”

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 supported

  Section 7.1 (page unavailable) reports reduced subsequent LTD in the nucleus accumbens shell of cocaine-sensitized mice, but describes a reduction in LTD magnitude rather than complete occlusion. Section 6.1 (page unavailable) specifies that the decrease in AMPA/NMDA ratio was measured after a cocaine challenge on withdrawal day 10–14, not simply after five days of cocaine; it attributes the decrease to reduced AMPAR number or function without establishing internalization. The cited passages do not identify the LTD as NMDAR-dependent. (LLM, conf=0.88)

  cites Wolf and Ferrario 2010 sourceExperimental — accuracy not yet measured

In the paper

“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.”

• Also stated in: § INDUCTION OF LTP AND LTD · plain

  “LTP and LTD are induced by specific patterns of activity (Malenka 1994).”

What the sources say

• ?Not checked — no full text of the sourcecites Malenka 1994 source

In the paper

“Ionotropic glutamate receptors do not work in isolation.They interact with many proteins of the postsynaptic density (PSD) (Elias and Nicoll 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Elias and Nicoll 2007 source

In the paper

“This design renders AM-PARs that contain GluA2 calcium-impermeable (Liu and Zukin 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Liu and Zukin 2007 source

In the paper

“It is important to note that NMDARs conduct currents only when glutamate is bound and the postsynaptic neuron is depolarized.”

In the paper

“In other words, both the pre-and postsynaptic neurons need to be active to open NMDARs.”

In the paper

“It is important to note that if LTP (or LTD) is caused by enhanced (or decreased) transmitter release, it requires that the postsynaptic cell somehow communicate to the presynaptic terminals and modify their function.”

In the paper

“After the application of an LTP induction protocol, these synapses “wake up” and become functional because of the insertion of AMPARs into their postsynaptic membrane (Isaac et al. 1995;Liao et al. 1995).”

What the sources say

• ?Not checked — no full text of the sourcecites Isaac et al. 1995 source
• ?Not checked — no full text of the sourcecites Liao et al. 1995 source

In the paper

“The number of glutamate receptors at a synapse (normally only a few dozens of receptors) can therefore be regulated through these interactions.”

In the paper

“This is because NMDARs on the synapses must be activated by synaptically released glutamate during the induction protocol.”

In the paper

“In addition, there are also forms of synaptic potentiation that are expressed by an exchange of GluA2-containing AMPARs in the synapse for GluA2-lacking AMPARs (Liu and Zukin 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Liu and Zukin 2007 source

In the paper

“An important property of these NMDARdependent forms of LTP and LTD is that they are input-or synapse-specific.”

In the paper

“It may be surprising that stimulation of the presynaptic axons alone is sufficient for LTP induction.”

In the paper

“LTP and LTD are induced by specific patterns of activity (Malenka 1994).”

What the sources say

• ?Not checked — no full text of the sourcecites Malenka 1994 source

In the paper

“If both stimulations, however, occur at once, an asymptote is reached, in which the resultant long-term change in synaptic strength can no longer be reliably predicted.”

In the paper

“If a presynaptic spike is repetitively elicited slightly before (e.g., 5 msec) the postsynaptic neuron is fired, the EPSP precedes the backpropagating action potential and such repetitive “pre-post” action potential firing can generate LTP.”

In the paper

“Taken together, these findings (and additional experiments that are not covered because of space limitations) make it very unlikely that LTP is associated with an increase in release probability or the amount of glutamate released from a presynaptic vesicle.”

In the paper

“If interactions with scaffolding proteins are manipulated through genetic interventions or the perfusion of dominant-negative proteins, LTP and LTD can be blocked (Lu ¨scher et al. 1999;Lu ¨thi et al. 1999;Collingridge and Isaac 2003).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lu ¨scher et al. 1999
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lu ¨thi et al. 1999
• ?Not checked — no full text of the sourcecites Collingridge and Isaac 2003 source

In the paper

“A large family of proteins associates with the AMPARs to regulate their mobility and biophysical properties as well as their stabilization within the PSD (see Sheng and Kim 2012).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Sheng and Kim 2012

In the paper

“Conversely, when the backprogating action potential is repetitively elicited before the presynaptic spike, “post-pre” firing, LTD is often observed.”

In the paper

“Presumably it is repeated occurrence of this smaller NMDAR-dependent Ca influx that triggers LTD induction.”

In the paper

“The phosphorylation of AMPAR subunits can cause an increase in the conductance of the AMPAR channel (Benke et al. 1998), another postsynaptic mechanism that contributes to at least the early phase of LTP.”

What the sources say

• ?Not checked — no full text of the sourcecites Benke et al. 1998 source

In the paper

“Because NMDAR-dependent calcium influx induces both LTP and LTD, the cell must have a way to decide whether to potentiate or depress a synaptic connection.”

In the paper

“The time window for such pairings is critical, such that the closer in time presynaptic and postsynaptic spikes are fired, the larger the magnitude of the plasticity induced.”

In the paper

“That is, only synapses that actively contribute to the induction process will undergo the plasticity.”

In the paper

“This means that application of MK-801 while activating a population of synapses leads to a gradual decrease of the postsynaptic currents generated by NMDARs, and the rate of this decrease directly correlates with the overall probability of release of the synapses being activated.”

In the paper

“Conversely, LTD can be induced by repeated activation of the presynaptic neuron at low frequencies without postsynaptic activity (see below).”

In the paper

“Just as with MK-801, the destaining curves were superimposable before and after tetanic induction of NMDAR-dependent LTP in CA1 neurons at 50 -100 Hz (Zakharenko et al. 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Zakharenko et al. 2001 source

In the paper

“More recently studies have shown that LTP and LTD can be elicited if action potentials in the pre-and postsynaptic neurons coincide with the appropriate timing.”

In the paper

“This provides relief of the Mg-dependent block of NMDARs, allowing calcium to enter the postsynaptic cell when the NMDARs are activated by the presynaptically released glutamate.”

In the paper

“The net result is weaker synapses that have difficulty generating LTP.”

In the paper

“In reality, the events of LTP expression and maintenance do not occur sequentially, and the first structural changes, such as the increase of the size of the PSD and spine growth, can be observed rapidly after induction.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Engert and Bonhoeffer 1999

In the paper

“Both local dendritic and nuclear transcription and somatic translation together are believed to synthesize the proteins required for the maintenance of functional and structural plasticity following the triggering of LTP.”

In the paper

“The slow GABA B receptor-mediated inhibitory postsynaptic potential (IPSP) can also be potentiated if the postsynaptic neuron is strongly depolarized (Huang et al. 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Huang et al. 2005 source

In the paper

“Although such structural changes in spines have been studied in some detail, they are not absolutely required for LTP, as synapses made”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites et al. 2010

In the paper

“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).”

What the sources say

• ?Not checked — no full text of the sourcecites Wang et al. 2007 source
• ?Not checked — no full text of the sourcecites Redondo and Morris 2011 source

In the paper

“In the ventral tegmental area, a similar form of plasticity called LTP GABA is induced by strong activation of NMDARs on dopamine neurons (Nugent et al. 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Nugent et al. 2007 source

In the paper

“In reality, the events of LTP expression and maintenance do not occur sequentially, and the first structural changes, such as the increase of the size of the PSD and spine growth, can be observed rapidly after induction.”

In the paper

“Not only does long-term plasticity cause structural changes in synapses, but the maintenance of the change in synaptic strength during LTP is protein synthesis -dependent.”

What the sources say

• ?Not checked — no full text of the sourcecites Sacktor 2008 source

In the paper

“There is now strong evidence that these two phosphatases do indeed play a role in LTD (Mulkey et al. 1993, 1994: Carroll et al. 2001), perhaps in part by influencing the phosphorylation state of AMPARs.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Mulkey et al. 1993, 1994
• ?Not checked — no full text of the sourcecites Carroll et al. 2001 source

In the paper

“Furthermore, at the ultrastructural level in electron micrographs, synapses that underwent LTP had enlarged PSDs that were often discontinuous (Toni et al. 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Toni et al. 2001 source

In the paper

“Not only does long-term plasticity cause structural changes in synapses, but the maintenance of the change in synaptic strength during LTP is protein synthesis -dependent.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Engert and Bonhoeffer 1999

In the paper

“The latter involves interactions with transcription factors, including cAMP response element -binding protein (CREB).”

What the sources say

• ?Not checked — no full text of the sourcecites Sacktor 2008 source

In the paper

“The release probability for GABA then increases through a still unknown mechanism involving activation of the cGMPdependent protein kinase, PKG.”

What the sources say

• ?Not checked — no full text of the sourcecites Nugent et al. 2007 source

In the paper

“Although such structural changes in spines have been studied in some detail, they are not absolutely required for LTP, as synapses made directly on the dendrites (i.e., shaft synapses) are capable of expressing and maintaining LTP.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites et al. 2010

In the paper

“In addition, in ways that remain to be determined, the increase in CaMKII activity contributes to the insertion of AMPARs (Ehlers 2000).”

What the sources say

• ?Not checked — no full text of the sourcecites Ehlers 2000 source

In the paper

“Nitric oxide in turn causes activation of guanylate cyclase and synthesis of cGMP in the synaptic terminals of inhibitory afferents onto dopamine neurons.”

What the sources say

• ?Not checked — no full text of the sourcecites Nugent et al. 2007 source

In the paper

“PKA, CaMKIV, protein kinase M-z, and extracellular signal -regulated kinase (ERK), as well as other signaling molecules, initiate protein synthesis either locally in the dendrites from prefabricated mRNA or by nuclear transcription (Sacktor 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Sacktor 2008 source

In the paper

“In the hippocampus, visual cortex, and optic tectum, a form of I-LTP dependent on brainderived neurotrophic factor (BDNF) has been described (Inagaki et al. 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Inagaki et al. 2008 source

In the paper

“For example, a single dose of a drug of abuse such as cocaine enhances excitatory transmission onto dopamine neurons of the ventral tegmental area (Ungless et al. 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Ungless et al. 2001 source

In the paper

“Conversely, blocking exocytosis abolishes LTP.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 3

In the paper

“Through coordination of functional changes in synaptic efficacy to structural changes in synapses, the reorganization of neural networks can be structurally maintained for long periods of time.”

In the paper

“NMDA receptors have a complex I -V curve because Mg blocks the pore at negative potentials.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 2

In the paper

“It is believed that these changes underlie the early cognitive decline observed in AD.”

In the paper

“Because of a major effort by a large number of investigators, the mechanisms underlying NMDAR-dependent LTP and LTD are understood in reasonable molecular detail.”

In the paper

“Calcium-permeable, GluA2-lacking AMPARs appear (Bellone and Lu ¨scher 2006), while NMDAR function is decreased.”

What the sources say

• ?Not checked — no full text of the sourcecites Bellone and Lüscher 2006 source

In the paper

“This causes the activity-dependent redistribution of AMPARs, a general mechanism for modifying synaptic strength in many neuronal cell types.”

In the paper

“When endocytosis is blocked with a dynamin dominant-negative peptide, LTD is inhibited.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 3

In the paper

“This preferentially activates phosphatases that dephosphorylate AMPA receptors, thus promoting receptor endocytosis.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 3

In the paper

“Synaptic strength correlates with spine volume and the area of the postsynaptic density (orange).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 4

In the paper

“In contrast, LTP at mossy fiber synapses onto CA3 neurons (green on blue) is NMDAR-independent.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 1

In the paper

“Calcium-permeable, GluA2-lacking AMPARs appear (Bellone and Lu ¨scher 2006), while NMDAR function is decreased.”

What the sources say

• ?Not checked — no full text of the sourcecites Bellone and Lüscher 2006 source

In the paper

“Strong activity paired with strong depolarization triggers LTP in part via CaMKII, receptor phosphorylation, and exocytosis.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 3

In the paper

“Within 30 min of triggering LTP (30 stimuli applied to the presynaptic axon at 10-sec intervals paired with depolarizing current injection into the postsynaptic neuron; black bar) of a synaptic connection in the hippocampus, new spines appear.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 4

In the paper

“As a consequence, normal NMDAR-dependent LTD is occluded.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 5

In the paper

“Weak activity of the presynaptic neuron leads to modest depolarization and calcium influx through NMDA receptors.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 3

In the paper

“As a result, the primary source for synaptic calcium entry shifts from NMDARs in naı ¨ve animals to GluA2-lacking AMPARs after a dose of an addictive drug.”

In the paper

“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.”

In the paper

“NMDA receptors are also permeable for calcium but only if the magnesium is expelled by a slight depolarization of the neuron.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 2

In the paper

“When glutamate binds to AMPA receptors, many sodium ions flow into the cell while only some potassium ions leave the neuron, causing a net depolarization of the membrane.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 2

In the paper

“LTP and LTD are induced by activation of NMDARs at synapses between CA3 and CA1 pyramidal neurons (blue and red).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 1

In the paper

“LTP can also lead to the appearance of new spines.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 4

In the paper

“Note that the PSD in potentiated synapses is often perforated.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fig. 4

In the paper

“As a consequence, the rules for subsequent activity-dependent plasticity are inverted (Mameli and Lu ¨scher 2011).”

What the sources say

• ?Not checked — no full text of the sourcecites Mameli and Lüscher 2011 source