IRSp53/BAIAP2 in dendritic spine development, NMDA receptor regulation, and psychiatric disorders

被引：60

作者：

Kang, Jaeseung ^{[1
]}

Park, Haram ^{[1
]}

Kim, Eunjoon ^{[1
,2
]}

机构：

[1] Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea

[2] Inst for Basic Sci Korea, Ctr Synapt Brain Dysfunct, Taejon 305701, South Korea

来源：

NEUROPHARMACOLOGY | 2016年 / 100卷

关键词：

Dendritic spine; Actin; Membrane; IRSp53; NMDA receptor; Psychiatric disorders; TYROSINE KINASE SUBSTRATE; LONG-TERM POTENTIATION; MEDIATED SYNAPTIC-TRANSMISSION; COPY-NUMBER VARIATION; INSULIN-RECEPTOR; ACTIN CYTOSKELETON; N-WASP; STRUCTURAL PLASTICITY; PROTEINS INTERACT; COMPLEX-FORMATION;

D O I：

10.1016/j.neuropharm.2015.06.019

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

IRSp53 (also known as BAIAP2) is a multi-domain scaffolding and adaptor protein that has been implicated in the regulation of membrane and actin dynamics at subcellular structures, including filo-podia and lamellipodia. Accumulating evidence indicates that IRSp53 is an abundant component of the postsynaptic density at excitatory synapses and an important regulator of actin-rich dendritic spines. In addition, IRSp53 has been implicated in diverse psychiatric disorders, including autism spectrum disorders, schizophrenia, and attention deficit/hyperactivity disorder. Mice lacking IRSp53 display enhanced NMDA (N-methyl-D-aspartate) receptor function accompanied by social and cognitive deficits, which are reversed by pharmacological suppression of NMDA receptor function. These results suggest the hypothesis that defective actin/membrane modulation in IRSp53-deficient dendritic spines may lead to social and cognitive deficits through NMDA receptor dysfunction. This article is part of the Special Issue entitled 'Synaptopathy - from Biology to Therapy'. (C) 2015 The Authors. Published by Elsevier Ltd.

引用

页码：27 / 39

页数：13

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