Altered NMDA receptor trafficking contributes to sleep deprivation-induced hippocampal synaptic and cognitive impairments

被引：81

作者：

Chen, C ^{[1
]}

Hardy, M

Zhang, J

LaHoste, GJ

Bazan, NG

机构：

[1] Louisiana State Univ, Hlth Sci Ctr, Sch Med, Ctr Neurosci, New Orleans, LA 70112 USA

[2] Univ New Orleans, Dept Psychol, New Orleans, LA 70148 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 340卷 / 02期

关键词：

long-term potentiation; rapid eye movement sleep; hippocampus-dependent contextual memory;

D O I：

10.1016/j.bbrc.2005.12.021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent evidence indicates that continuous wakefulness (sleep deprivation, SD) causes impairments in behavioral performance and hippocampal long-term potentiation (LTP) in animals. However, the mechanisms by which SD impairs long-term synaptic plasticity and cognitive function are not clear. Here, we report that 24-h SD in mice results in impaired hippocampus-dependent contextual memory and LTP and, unexpectedly, in reductions of the surface expression of NMDA receptor (NMDAR) subunit NR1 and NMDAR-mediated excitatory post-synaptic currents at hippocampal perforant path-dentate granule cell synapses. The results suggest that the reduction of functional NMDAR in hippocampal neurons may underlie the SD-induced deficits in hippocampus-dependent contextual memory and long-term synaptic plasticity. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：435 / 440

页数：6

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