期刊
PSYCHONEUROENDOCRINOLOGY
卷 40, 期 -, 页码 119-122出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2013.11.009
关键词
Stress; Cognitive deficit; Prefrontal cortex; Ketamine; NMDA receptors; Set-shifting
资金
- Depresja-mechanizmy-terapia [POIG.01.01.02-12-004/09]
- European Union from the European Fund of Regional Development (EFRD)
- Statutory Activity of the Institute of Pharmacology, Polish Academy of Sciences
Chronic stress produces both morphological and functional alternations of the rat medial prefrontal cortex (mPFC). N-methyl-D-aspartic acid (NMDA) glutamate receptor inhibition may alleviate such stress-induced dendritic reorganization in the mPFC. However, it is unknown whether administration of a NMDAR antagonist would also prevent alterations in PFC-mediated cognitive functions. Here, we investigated whether administration of ketamine, the noncompetitive antagonist of NMDA receptors before each stress session would prevent cognitive impairments in a rat model of prefrontal cortex (PFC)-dependent attentional set-shifting task (ASST), a measure of cognitive flexibility. Repeated restraint stress (1 h daily for 7 days) significantly and specifically impaired extra-dimensional (ED) set-shifting ability of rats. Pretreatment with ketamine (10 mg/kg, IP) completely and specifically prevented this stress-induced cognitive inflexibility. The present study demonstrates procognitive efficacy of ketamine in an animal stress model, which confirms and extends the role of the NMDA receptors in mediating stress-evoked prefrontal dysfunctions. (C) 2013 Elsevier Ltd. All rights reserved.
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