基础医学与临床 ›› 2011, Vol. 31 ›› Issue (8): 879-883.

• 研究论文 • 上一篇    下一篇

抑郁模型大鼠杏仁核神经元凋亡增加

田艳霞,王海涛,李冉,阚泉,高俊玲   

  1. 华北煤炭医学院
  • 收稿日期:2010-06-18 修回日期:2010-09-07 出版日期:2011-08-05 发布日期:2011-07-13
  • 通讯作者: 高俊玲 E-mail:Junlinggao@163.com
  • 基金资助:
    省自然科学基金

Increased Apoptosis in amygdala neurons of depression model rats

Yan-xia TIAN1,Hai-tao WANG2,Ran LI2,Quan KAN2,Jun-ling GAO1   

  1. 1. North China Coal Medical college
    2.
  • Received:2010-06-18 Revised:2010-09-07 Online:2011-08-05 Published:2011-07-13
  • Contact: Jun-ling GAO E-mail:Junlinggao@163.com

摘要: 目的 观察细胞色素C(Cyt C)和凋亡相关基因bax在抑郁模型大鼠杏仁核神经元的表达,探讨抑郁症杏仁核神经元凋亡的机制。 方法 将Wistar大鼠随机分为对照组和模型组,每组15只。用慢性强迫游泳(4周)制备慢性强迫游泳应激抑郁模型。用糖水偏好实验、开场实验和Morris水迷宫检测大鼠行为学。用TUNEL和流式细胞术检测神经元凋亡和凋亡率,Western Blot检测Cyt C和Bax蛋白的表达,RT-PCR检测bax mRNA表达。 结果 模型组糖水消耗量、糖水偏好百分比和直立次数低于对照组(P<0.01或P<0.05);逃避潜伏期高于对照组(P<0.01);模型组和对照组凋亡细胞阳性率分别为24.08%±4.30%和3.08%±0.91%,凋亡率分别为17.14%±2.71%和3.34%±0.80%。凋亡相关基因bax转录和Bax蛋白以及Cyt C蛋白明显高于对照组(P<0.01)。结论 抑郁模型大鼠杏仁核存在明显的神经元凋亡,Bax上调和Cyt C释放可能是抑郁患者杏仁核神经元凋亡的机制之一。

关键词: 慢性强迫游泳应激, 杏仁核, 凋亡, 细胞色素C, Bax, 大鼠

Abstract: Objective To observe the expression of Cytochrome C and apoptosis-related gene bax in amygdala of depression model rats. Methods Male Wistar rats were randomly divided into control group and model group. Chronic forced swimming stress was carried out to set up the rat depression model. TUNEL-staining and double-labeled flow cytometry (FCM) were employed for the detection and quantification of the apoptotic cells in the amygdala. The expression of Cytochrome C and gene bax was detected using Western blotting and RT-PCR. Results The consumption of sucrose, preference of sucrose, erect quantity and escape latency of model rat were signficantly decreased compared with of the normal group (P<0.01, P<0.05). The percentage of TUNEL-positive cell, the apoptotic cell rate and the expression of Cytochrome C and gene bax of model group were higher than those of control group respectively (P<0.01). Conclusion Apoptosis was increased in amygdala neurons of depression model rats, and bax is up-regulated and promotes the releasing of Cytochrome C.

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