Altered NMDA receptor trafficking contributes to sleep deprivation-induced hippocampal synaptic and cognitive impairments.
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.
Chen
Chu
C
Neuroscience Center, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. cchen@lsuhsc.edu
Hardy
Mattie
M
Zhang
Jian
J
LaHoste
Gerald J
GJ
Bazan
Nicolas G
NG
D000818:Animals; D003072:Cognition Disorders / Q000378:metabolism* / Q000503:physiopathology; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008568:Memory / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism* / Q000502:physiology; D012892:Sleep Deprivation / Q000378:metabolism* / Q000503:physiopathology; D013569:Synapses / Q000378:metabolism*
D016194:Receptors, N-Methyl-D-Aspartate