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Enhanced NMDA receptor-mediated synaptic transmission, enhanced long-term potentiation, and impaired learning and memory in mice lacking IRSp53

Cited 95 time in Web of Science Cited 97 time in Scopus
Authors
Kim, Myoung-Hwan; Choi, Jeonghoon; Yang, Jinhee; Chung, Woosuk; Paik, Sang Kyoo; Han, Seungnam; Bae, Young-Soo; Seo, Jinsoo; Choi, Se-Young; Kim, Eunjoon; Bae, Yong Chul; Cho, Suk-Hee; Won, Hyejung; Kim, Karam; Kim, Ji-Hyun
Issue Date
2009
Publisher
Society for Neuroscience
Citation
Journal of Neuroscience; Vol.29, No.5, pp.1586-1595
Keywords
ActinSynapsePSD-95IRSp53Learning and memoryLTP
Abstract
IRSp53 is an adaptor protein that acts downstream of Rac and Cdc42 small GTPases and is implicated in the regulation of membrane deformation and actin filament assembly. In neurons, IRSp53 is an abundant postsynaptic protein and regulates actin-rich dendritic spines; however, its in vivo functions have not been explored. We characterized transgenic mice deficient of IRSp53 expression. Unexpectedly, IRSp53 -/- neurons do not show significant changes in the density and ultrastructural morphologies of dendritic spines. Instead, IRSp53 -/- neurons exhibit reduced AMPA/NMDA ratio of excitatory synaptic transmission and a selective increase in NMDA but not AMPA receptor-mediated transmission. IRSp53 -/- hippocampal slices show a markedly enhanced long-term potentiation (LTP) with no changes in long-term depression. LTP-inducing theta burst stimulation enhances NMDA receptor-mediated transmission. Spatial learning and novel object recognition are impaired in IRSp53 -/- mice. These results suggest that IRSp53 is involved in the regulation of NMDA receptor-mediated excitatory synaptic transmission, LTP, and learning and memory behaviors. Copyright ⓒ 2009 Society for Neuroscience.
ISSN
0270-6474
Language
English
URI
http://hdl.handle.net/10371/80841
DOI
https://doi.org/10.1523/JNEUROSCI.4306-08.2009
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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