IRSp53/BAIAP2 in dendritic spine development, NMDA receptor regulation, and psychiatric disorders
Cited 27 time in
Cited 31 time in
1,426 Viewed
251 Downloaded
-
Title
- IRSp53/BAIAP2 in dendritic spine development, NMDA receptor regulation, and psychiatric disorders
-
Author(s)
- Jaeseung Kang; Haram Park; Eunjoon Kim
-
Subject
- Actin, ; Dendritic spine, ; IRSp53, ; Membrane, ; NMDA receptor, ; Psychiatric disorders
-
Publication Date
- 2016-01
-
Journal
- NEUROPHARMACOLOGY, v.100, pp.27 - 39
-
Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
-
Abstract
- 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 filopodia 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'. © 2015 The Authors. All rights reserved
-
URI
- https://pr.ibs.re.kr/handle/8788114/1820
-
DOI
- 10.1016/j.neuropharm.2015.06.019
-
ISSN
- 0028-3908
-
Appears in Collections:
- Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
- Files in This Item:
-
2015_122.pdfDownload
-
- Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.