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短期暴露于丰富环境可挽救慢性应激诱导的海马突触可塑性受损、焦虑及记忆缺陷。

Short-term exposure to enriched environment rescues chronic stress-induced impaired hippocampal synaptic plasticity, anxiety, and memory deficits.

作者信息

Bhagya Venkanna Rao, Srikumar Bettadapura N, Veena Jayagopalan, Shankaranarayana Rao Byrathnahalli S

机构信息

Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bengaluru, India.

出版信息

J Neurosci Res. 2017 Aug;95(8):1602-1610. doi: 10.1002/jnr.23992. Epub 2016 Nov 16.

Abstract

Exposure to prolonged stress results in structural and functional alterations in the hippocampus including reduced long-term potentiation (LTP), neurogenesis, spatial learning and working memory impairments, and enhanced anxiety-like behavior. On the other hand, enriched environment (EE) has beneficial effects on hippocampal structure and function, such as improved memory, increased hippocampal neurogenesis, and progressive synaptic plasticity. It is unclear whether exposure to short-term EE for 10 days can overcome restraint stress-induced cognitive deficits and impaired hippocampal plasticity. Consequently, the present study explored the beneficial effects of short-term EE on chronic stress-induced impaired LTP, working memory, and anxiety-like behavior. Male Wistar rats were subjected to chronic restraint stress (6 hr/day) over a period of 21 days, and then they were exposed to EE (6 hr/day) for 10 days. Restraint stress reduced hippocampal CA1-LTP, increased anxiety-like symptoms in elevated plus maze, and impaired working memory in T-maze task. Remarkably, EE facilitated hippocampal LTP, improved working memory performance, and completely overcame the effect of chronic stress on anxiety behavior. In conclusion, exposure to EE can bring out positive effects on synaptic plasticity in the hippocampus and thereby elicit its beneficial effects on cognitive functions. © 2016 Wiley Periodicals, Inc.

摘要

长期暴露于应激状态会导致海马体出现结构和功能改变,包括长时程增强(LTP)降低、神经发生减少、空间学习和工作记忆受损以及焦虑样行为增强。另一方面,丰富环境(EE)对海马体的结构和功能具有有益影响,如改善记忆、增加海马体神经发生以及渐进性突触可塑性。目前尚不清楚短期(10天)暴露于EE是否能够克服束缚应激诱导的认知缺陷和海马体可塑性受损。因此,本研究探讨了短期EE对慢性应激诱导的LTP受损、工作记忆和焦虑样行为的有益影响。雄性Wistar大鼠在21天的时间里每天接受6小时的慢性束缚应激,然后再接受10天的EE(每天6小时)。束缚应激降低了海马体CA1区的LTP,增加了高架十字迷宫中的焦虑样症状,并损害了T迷宫任务中的工作记忆。值得注意的是,EE促进了海马体LTP,改善了工作记忆表现,并完全克服了慢性应激对焦虑行为的影响。总之,暴露于EE可对海马体的突触可塑性产生积极影响,从而对认知功能产生有益作用。© 2016威利期刊公司

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