A critical role for PSD-95/AKAP interactions in endocytosis of synaptic AMPA receptors.

Abstract:

:The endocytosis of AMPA receptors (AMPARs) underlies several forms of synaptic plasticity, including NMDA receptor (NMDAR)-dependent long-term depression (LTD), but the molecular mechanisms responsible for this trafficking remain unknown. We found that PSD-95, a major postsynaptic density protein, is important for NMDAR-triggered endocytosis of synaptic AMPARs in rat neuron cultures because of its binding to A kinase-anchoring protein 150 (AKAP150), a scaffold for specific protein kinases and phosphatases. Knockdown of PSD-95 with shRNA blocked NMDAR-triggered, but not constitutive or mGluR-triggered, endocytosis of AMPARs. Deletion of PSD-95's Src homology 3 and guanylate kinase-like domains, as well as a point mutation (L460P), both of which inhibit binding of PSD-95 to AKAP150, also blocked NMDAR-triggered AMPAR endocytosis. Furthermore, expression of a mutant AKAP150 that does not bind calcineurin inhibited this NMDAR-triggered trafficking event. Our results suggest that PSD-95's interaction with AKAP150 is critical for NMDAR-triggered AMPAR endocytosis and LTD, possibly because these scaffolds position calcineurin in the appropriate subsynaptic domain.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Bhattacharyya S,Biou V,Xu W,Schlüter O,Malenka RC

doi

10.1038/nn.2249

subject

Has Abstract

pub_date

2009-02-01 00:00:00

pages

172-81

issue

2

eissn

1097-6256

issn

1546-1726

pii

nn.2249

journal_volume

12

pub_type

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