An essential role for PICK1 in NMDA receptor-dependent bidirectional synaptic plasticity

被引：148

作者：

Terashima, Akira ^{[1
,2
]}

Pelkey, Kenneth A. ^{[3
]}

Rah, Jong-Cheol ^{[1
]}

Suh, Young Ho ^{[4
]}

Roche, Katherine W. ^{[4
]}

Collingridge, Graham L. ^{[2
]}

McBain, Chris J. ^{[3
]}

Isaac, John T. R. ^{[1
,2
]}

机构：

[1] Natl Inst Neurol Disorders & Stroke, Dev Synapt Plast Sect, NIH, Bethesda, MD 20892 USA

[2] Univ Bristol, Sch Med Sci, Dept Anat, MRC Ctr Synspt Plat, Bristol BS8 1TD, Avon, England

[3] NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA

[4] Natl Inst Neurol Disorders & Stroke, Receptor Biol Unit, NIH, Bethesda, MD 20892 USA

来源：

NEURON | 2008年 / 57卷 / 06期

基金：

英国医学研究理事会; 英国惠康基金;

关键词：

D O I：

10.1016/j.neuron.2008.01.028

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

PICK1 is a calcium-sensing, PDZ domain-containing protein that interacts with GluR2 and GluR3 AMPA receptor (AMPAR) subunits and regulates their trafficking. Although PICK1 has been principally implicated in long-term depression (LTD), PICK1 overexpression in CA1 pyramidal neurons causes a CaMK- and PKC-dependent potentiation of AMPAR-mediated transmission and an increase in synaptic GluR2-lacking AMPARs, mechanisms associated with NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here, we directly tested whether PICK1 participates in both hippocampal NMDAR-dependent LTP and LTD. We show that the PICK1 potentiation of AMPAR-mediated transmission is NMDAR dependent and fully occludes LTP. Conversely, blockade of PICK1 PDZ interactions or lack of PICK1 prevents LTP. These observations demonstrate an important role for PICK1 in LTP. In addition, deletion of PICK1 or blockade of PICK1 PDZ binding prevented NMDAR-dependent LTD. Thus, PICK1 plays a critical role in bidirectional NMDAR-dependent long-term synaptic plasticity in the hippocampus.

引用

页码：872 / 882

页数：11

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