GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity

Duprat, Fabrice; Daw, Michael I.; Lim, Wonil; Collingridge, Graham L.; Isaac, John T.R.

doi:10.1098/rstb.2002.1215

Cited by 24 publications

(15 citation statements)

References 47 publications

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“…6 D ). These results are surprising, as a central tenet for the function of PICK1 has been that it mediates its effects on AMPAR trafficking through direct association with GluA2 (Xia et al, 1999; Kim et al, 2001; Perez et al, 2001; Duprat et al, 2003; Dev et al, 2004; Terashima et al, 2004; Hanley, 2008; Terashima et al, 2008; Thorsen et al, 2010). Therefore, to further test the importance of the direct interaction between GluA2 and the PICK1 PDZ domain we tested the effects of an additional PDZ domain mutant (K27E; Fig.…”

Section: Resultsmentioning

confidence: 97%

“…This finding suggests that, in contrast to a predominant model (Daw et al, 2000; Kim et al, 2001; Hanley, 2008), direct binding of PICK1 to AMPAR subunits is not required during LTD. Much of the previous work that suggested a critical role for direct PICK1-GluA2/3 interactions in LTD depended on the postsynaptic loading or expression of a peptide that disrupted this interaction. However, the results using such peptides have been inconsistent, with reports of either a block of LTD or a minimal effect on LTD in CA1 pyramidal cells (Daw et al, 2000; Xia et al, 2000; Kim et al, 2001; Duprat et al, 2003; Terashima et al, 2008; Thorsen et al, 2010). The reported effects of such peptides on basal synaptic transmission have been similarly inconsistent (Daw et al, 2000; Kim et al, 2001; Terashima et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

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Calcium Binding to PICK1 Is Essential for the Intracellular Retention of AMPA Receptors Underlying Long-Term Depression

Citri¹,

Bhattacharyya²,

Ma³

et al. 2010

J. Neurosci.

107

160

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Section: Resultsmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Calcium Binding to PICK1 Is Essential for the Intracellular Retention of AMPA Receptors Underlying Long-Term Depression

Citri¹,

Bhattacharyya²,

Ma³

et al. 2010

J. Neurosci.

107

160

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“…This rundown is dependent on afferent synaptic activity (Luscher et al, 1999) and is reversed by periods of synaptic inactivity (Duprat et al, 2003). This contrasts with the enhancement of synaptic transmission by PKMζ, which is independent of afferent stimulation (Ling et al, 2006).…”

Section: Resultsmentioning

confidence: 99%

PKMζ Maintains Late Long-Term Potentiation byN-Ethylmaleimide-Sensitive Factor/GluR2-Dependent Trafficking of Postsynaptic AMPA Receptors

Yao¹,

Kelly²,

Sajikumar³

et al. 2008

J. Neurosci.

242

276

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Although the maintenance mechanism of late long-term potentiation (LTP) is critical for the storage of long-term memory, the expression mechanism of synaptic enhancement during late-LTP is unknown. The autonomously active protein kinase C isoform, protein kinase M (PKM), is a core molecule maintaining late-LTP. Here we show that PKM maintains late-LTP through persistent N-ethylmaleimide-sensitive factor (NSF)/glutamate receptor subunit 2 (GluR2)-dependent trafficking of AMPA receptors (AMPARs) to the synapse. Intracellular perfusion of PKM into CA1 pyramidal cells causes potentiation of postsynaptic AMPAR responses; this synaptic enhancement is mediated through NSF/GluR2 interactions but not vesicle-associated membrane protein-dependent exocytosis. PKM may act through NSF to release GluR2-containing receptors from a reserve pool held at extrasynaptic sites by protein interacting with C-kinase 1 (PICK1), because disrupting GluR2/PICK1 interactions mimic and occlude PKM-mediated AMPAR potentiation. During LTP maintenance, PKM directs AMPAR trafficking, as measured by NSF/GluR2-dependent increases of GluR2/3-containing receptors in synaptosomal fractions from tetanized slices. Blocking this trafficking mechanism reverses established late-LTP and persistent potentiation at synapses that have undergone synaptic tagging and capture. Thus, PKM maintains late-LTP by persistently modifying NSF/GluR2-dependent AMPAR trafficking to favor receptor insertion into postsynaptic sites.

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“…Intracellular introduction of a 10 amino acid peptide sequence (pep2m) that blocks the interaction of NSF and GluR2 causes a rundown of AMPA receptor-mediated EPSCs, suggesting that the NSF/GluR2 interaction is necessary to maintain synaptic transmission (23,(26)(27)(28). However, the EPSC can recover fully if synaptic activation is halted (29), suggesting that an NSF-independent mechanism traffics AMPA receptors in the absence of synaptic activity. It is possible that in the present study, the AMPA receptors formed on reintroduction of GluR2 subunits lacking the NSF-binding domain use this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Synaptic AMPA receptor subunit trafficking is independent of the C terminus in the GluR2-lacking mouse

Panicker

Brown²

2008

Proc. Natl. Acad. Sci. U.S.A.

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Glutamate is the primary excitatory neurotransmitter in the brain, and ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) type glutamate receptors mediate most fast synaptic transmission. AMPA receptors are tetrameric assemblies composed from four possible subunits (GluR1-4). In hippocampal pyramidal cells, AMPA receptors are heteromeric receptors containing the GluR2 subunit and either GluR1 or GluR3. It is generally accepted that the trafficking of GluR1/GluR2 receptors to synapses requires activity, whereas GluR2/GluR3 receptors traffic constitutively. It has been suggested that the trafficking is governed by the cytoplasmic C termini of the subunits. Because the basis for this theory relied on the introduction of unnatural, homomeric, calcium-permeable AMPA receptors, we have used the GluR2 ؊/؊ knock out mouse to determine whether the expression of mutated forms of GluR2 can rescue WT synaptic responses. We find that GluR2, lacking its entire C terminus, or a GluR2 chimera containing the C terminus of GluR1, is capable of trafficking to the synapse in the absence of activity. These findings suggest that the GluR2 C terminus is not required for GluR2 synaptic insertion.

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GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity

Cited by 24 publications

References 47 publications

Calcium Binding to PICK1 Is Essential for the Intracellular Retention of AMPA Receptors Underlying Long-Term Depression

Calcium Binding to PICK1 Is Essential for the Intracellular Retention of AMPA Receptors Underlying Long-Term Depression

PKMζ Maintains Late Long-Term Potentiation byN-Ethylmaleimide-Sensitive Factor/GluR2-Dependent Trafficking of Postsynaptic AMPA Receptors

Synaptic AMPA receptor subunit trafficking is independent of the C terminus in the GluR2-lacking mouse

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