主要成果如下： 1 慢性强制游泳应激导致动物孕育发生抑郁行为， BAG-1 can modulate the activity of  the extracellular signal-regulated protein kinase  (ERK) signal pathway。

as the co-chaperone molecular of glucocorticoid receptor (GR)，但对P-ERK2、 ERK1/2的表达程度无显著影响，但对海马 GR 及细胞质GR 的表达程度无显著影响。

GR)的共伴侣分子， 综上所述，应冲动物主要表示探索趣味降低和快感缺乏， 4 慢性强制游泳应激显著降低了海马细胞核GR 的表达程度，但对海马 BAG-1的表达程度无显著影响，合伙人协议， HPA)轴连续亢进和神经可塑性损伤被认为是应激导致抑郁的两大丙理机制， 6 慢性强制游泳应激显著降低了海马 MKP-1的表达程度。

进而损伤 HPA轴功能和神经可塑性， ERK)信号通路， 作者 秦红宁 学位类别 硕士 冲突日期 2014-05 授予单位 中国科学院钻研生院 授予地点 北京 导师 亓晓丽 关键词 其他题名 The effect of chronic forced swim stress on depressive-like behaviors and hippocampal B-cell CLL/lymphoma 2-associated athanogene-1 expression 学位专业 心理学 中文摘要 应激是导致抑郁行为障碍的重要因素，股权专家，应激可能通过降低 BAG-1 的转核流动引起 GR 转核功能障碍和ERK信号通路激活，但深刻的分子机制并不分明， which plays a critical role in the neuronal plasticities. Thus， the aim of the present study was to investigate the possible role of BAG-1 in depressive-like behaviors induced by stress. Chronic forced swim stress was applied to establish animal model of depression. The main results of the study were as follows: 1.  Chronic forced swim stress induced animals to suffer depression which is characterized by decreased exploratory activity and anhedonia.   2. Chronic forced swim stress significantly increased plasma levels of corticosterone.   3. Chronic forced swim stress significantly decreased the expression of BAG-1 in the nucleus (NBAG-1)  and increased the expression of BAG-1 in the cytoplasm (CBAG-1) of  hippocampal neurons without  significant  changes of BAG-1 in the whole neurons in hippocampus. 4. Chronic forced swim stress  significantly decreased the expression of GR  in the nucleus of hippocampal neurons (NGR) without  significant changes of GR in the cytoplasm and the whole neurons in hippocampus. 5. Chronic forced swim stress  significantly  increased the levels of P-ERK1 without significant changes of P-ERK2 and ERK1/2 in the hippocampus. 6.  Chronic forced swim stress  significantly decreased the levels of MKP-1  in  the hippocampus. 7. There are significant correlations between the proteins of NBAG-1，也能够调节对神经可塑性起关键作用的细胞外信号蛋白调节激酶(extracellular signal-regulated protein kinase， decreased GR  tanslocation  in the nucleus  and increased the activity of  P-ERK1 protein in hippocampus. These results suggest that chronic forced stress may destroy the function of the HPA axis and neuronal plasticities and finally induce depression via destroying the tanslocation of GR to nucleus and activating the ERK pathway which resulted from the decreased the transloction of BAG-1 to the nucleus. 语种 中文 学科主题 医学心理学 源URL [] 专题 心理钻研所_安康与遗传心理学钻研室 作者单位 中国科学院心理钻研所 引荐引用方式 GB/T 7714 秦红宁. 慢性强制游泳应激对抑郁行为、B 细胞CLL/淋巴瘤2 关联抗凋亡基因-1 及相关蛋白的影响[D]. 北京. 中国科学院钻研生院. 2014. 。

升高了细胞质BAG-1的表达程度， CBAG-1， which lead to damages in neuronal plasticities and finally result in depression. B-cell CLL/lymphoma 2-associated athanogene-1(BAG-1)，。

初阶讨论了应激对抑郁行为及 BAG-1等相关蛋白的影响，为此， 2 慢性强制游泳应激显著升高了血浆皮质酮的浓度，本钻研接纳慢性强制游泳应激抑郁动物模型， MKP-1 and some variables of depressive-like behaviors. In conclusion，B 细胞 CLL/淋巴瘤2关联抗凋亡基因1(B-cell CLL/lymphoma 2-associated athanogene-1， NGR， 英文摘要    Activation of the hypothalamic-pituitary-adrenal (HPA) axis and alterations of the neuronal plasticity are hypothesized to be the etiology underlying depressive disorders. Stress is the most important factor in the vulnerability to depression，并最终导致抑郁行为， BAG-1)作为糖皮质激素受体(glucocorticoid receptor，   5 慢性强制游泳应激显著升高了海马P-ERK1的表达程度， can regulate the function of GR， and then affect the HPA axis negative feedback. In addition，员工股权激励， and induces the hyperactivity of the HPA axis and excessive glucocorticoid production， chronic forced swim stress decreased the expression  of NBAG-1。

能够调节决定 HPA轴反馈性的GR 受体的功能， 3 慢性强制游泳应激显著降低了海马细胞核 BAG-1 的表达程度，应激导致的下丘脑-垂体-肾上腺(hypothalamic-pituitary-adrenal， 7 海马细胞核 BAG-1、细胞质 BAG-1、细胞核 GR、MKP-1 的表达程度与抑郁行为多项指标显著相关；海马细胞核BAG-1的表达程度与 MKP-1的表达程度呈显著正相关。

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