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暴露于丰富环境可恢复海马体中新生细胞的存活和分化,并改善慢性应激大鼠的抑郁症状。

Exposure to enriched environment restores the survival and differentiation of new born cells in the hippocampus and ameliorates depressive symptoms in chronically stressed rats.

作者信息

Veena J, Srikumar B N, Raju T R, Shankaranarayana Rao B S

机构信息

Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), PB # 2900, Hosur Road, Bangalore 560 029, India.

出版信息

Neurosci Lett. 2009 May 22;455(3):178-82. doi: 10.1016/j.neulet.2009.03.059. Epub 2009 Mar 21.

Abstract

Chronic stress decreases neurogenesis in the adult brain, while exposure to enriched environment (EE) increases it. Recent studies demonstrate the ability of EE to ameliorate stress-induced behavioral deficits. Whether a restored neurogenesis contributes to these effects of EE is unknown. Recently, we demonstrated that EE following restraint stress restores cell proliferation in the dentate gyrus (DG), hippocampal volume and learning. In the current study, we examine the effects of EE following stress on survival and differentiation of the progenitor cells in the DG and behavioral depression using the forced swim test (FST) and sucrose consumption test (SCT). Adult male Wistar rats were subjected to 21 days of restraint stress followed by housing in either standard or enriched conditions (10 days, 6h/day). Survival and differentiation of BrdU-labeled cells were evaluated 31 days post-BrdU administration. Stress decreased the survival and differentiation of progenitor cells, which was ameliorated by EE. Also the percentage of BrdU-ir cells that did not co-localize with NeuN or S100beta was significantly greater in the stressed rats and was restored by EE. Stress increased immobility in FST and decreased sucrose preference in the SCT, and these behaviors were ameliorated by EE. Adult neurogenesis is thought to be linked to learning and memory and in mediating antidepressant effect. Taken together with our earlier report that EE restores stress-induced impairment in learning and cytogenesis, the current results indicate that the reversal of adult neurogenesis could be one of the mechanisms involved in the amelioration of stress-induced deficits.

摘要

慢性应激会减少成年大脑中的神经发生,而置身于丰富环境(EE)中则会增加神经发生。最近的研究表明,丰富环境有能力改善应激诱导的行为缺陷。神经发生的恢复是否促成了丰富环境的这些作用尚不清楚。最近,我们证明了束缚应激后的丰富环境可恢复齿状回(DG)中的细胞增殖、海马体积和学习能力。在本研究中,我们使用强迫游泳试验(FST)和蔗糖消耗试验(SCT),研究应激后的丰富环境对DG中祖细胞存活和分化以及行为性抑郁的影响。成年雄性Wistar大鼠经受21天的束缚应激,随后分别饲养于标准条件或丰富条件下(10天,每天6小时)。在给予溴脱氧尿苷(BrdU)后31天评估BrdU标记细胞的存活和分化情况。应激降低了祖细胞的存活和分化,而丰富环境则改善了这一情况。此外,在应激大鼠中,不与NeuN或S100β共定位的BrdU免疫反应细胞的百分比显著更高,而丰富环境使其恢复正常。应激增加了FST中的不动时间,并降低了SCT中的蔗糖偏好,而丰富环境改善了这些行为。成年神经发生被认为与学习和记忆有关,并介导抗抑郁作用。结合我们之前的报告,即丰富环境可恢复应激诱导的学习和细胞生成损伤,目前的结果表明,成年神经发生的逆转可能是参与改善应激诱导缺陷的机制之一。

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