Abstract:
:Although numerous studies have indicated that chronic stress causes cognitive dysfunction with the impairment of synaptic structures and functions, the relationship between cognitive deficits induced by repeated restraint stress and the level of NMDA receptors in the subregion of the hippocampus has been relatively unknown until now. In this study, 3-week-old male Sprague-Dawley rats were exposed to repeated restraint stress for seven consecutive days, their cognitive functions were evaluated through behavioral tests, and then they were sacrificed for electrophysiological, morphological, and biochemical assays. Chronic repeated restraint stress led to cognitive and electrophysiological impairments, with a reduced density of dendritic spines. We also found that the protein level of NMDA receptors only increased in the hippocampal CA3 region. Nevertheless, repeated restraint stress-induced cognitive and synaptic dysfunction were effectively reversed by Ro25-6981, an inhibitor of the GluN2B receptor. These findings suggest that repeated restraint stress-induced synaptic and cognitive deficits are probably mediated through NMDA receptors.
journal_name
Front Mol Neuroscijournal_title
Frontiers in molecular neuroscienceauthors
Sun DS,Zhong G,Cao HX,Hu Y,Hong XY,Li T,Li X,Liu Q,Wang Q,Ke D,Liu GP,Ma RH,Luo DJdoi
10.3389/fnmol.2020.552787subject
Has Abstractpub_date
2020-10-19 00:00:00pages
552787issn
1662-5099journal_volume
13pub_type
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