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作 者:曹岩菁[1] 吴佳丽[1] 李鹏[1] 林萍[1] 冯莉[1] 王琴[1] 任谦[1] 谢晓峰 CaO Yanjing;Wu Jiali;Li Peng;Lin Ping;Feng Li;Wang Qin;Ren Qian;Xie Xiaofeng(Department of general Practice,the Third Hospital of Hangzhou,Hangzhou,310009)
机构地区:[1]杭州市第三人民医院全科医学科,浙江杭州310009
出 处:《温州医科大学学报》2018年第11期801-806,812,共7页Journal of Wenzhou Medical University
基 金:浙江省卫生厅科研基金资助项目(2014KYB198);杭州市卫生局科研基金资助项目(2014A21)
摘 要:目的:探讨大鼠在慢性全脑缺血的状态下,其与递质相关的不同的囊泡转运体,如谷氨酸囊泡转运体(vGluTs)、乙酰胆碱囊泡转运体(vAChT)、氨基丁酸转运蛋白(vGAT)在海马CA1-3区内表达的特点。方法:采用BCCAO法建立血管性痴呆动物模型,Morris水迷宫实验和T-迷宫延迟交替实验检测大鼠学习记忆能力,Western blot及免疫组织化学法检测痴呆大鼠vGluTs、vAChT、vGAT在海马CA1-3区中表达的特点。结果:Morris实验中,痴呆组大鼠的逃避潜伏期时间明显延长(P<0.05);穿越平台次数明显减少(P< 0.05);在象限中游行距离的百分比明显缩短(P<0.01)。T-迷宫实验中,痴呆组大鼠延缓交替作业的错误率明显增高(P<0.01)。与正常及对照组比,痴呆组大鼠海马CA1-3区vGluT1和vGluT3的水平明显降低(P<0.01)。与正常及对照组比,痴呆组大鼠海马CA1-3区vAChT的表达有所下降(P<0.01)。与正常及对照组相比,痴呆组大鼠vGluT1和vGluT3阳性神经元的数量在海马CA1-3区表达下降,vAChT阳性神经元的数量在海马CA1-3中表达也明显下降(P<0.01)。结论:谷氨酸能和胆碱能囊泡转运体功能缺陷、谷氨酸中枢胆碱能递质间的不平衡、神经元的缺失、CA1-3区海马信息环路的破坏是慢性全脑缺血状态下大鼠产生认知功能障碍的主要原因。Objective: To investigate the expression of different vesicles transporter (different synapses) vGluTs, vAChT and vGAT in the hippocampal CA1-3 region in rats with chronic global cerebral ischemia. Methods: VaD animal model was established by BCCAO method, Western blot and immunofuorescence were used to detect the expression of vGluTs, vAChT and vGAT in hippocampal CA1-3. Results: In the Morris test, the escape latency of VaD rats was signifcantly extended compared with sham and control animals (P〈0.05). The percentage of searching time in the VaD group was signifcantly reduced (P〈0.05) and the searching distance in target quadrant was signifcantly decreased (P〈0.01). In the T-maze test: the error rate of the delayed operation of VaD rats was signifcantly increased (P〈0.01). The levels of vGluT1 and vGluT3 in the hippocampal CA1-3 re-gion of VaD rats were signifcantly lower than those in the sham and control groups (P〈0.01). Compared with the sham and control groups, the expression of vAChT in the hippocampal CA1-3 region of VaD rats was decreased (P〈0.01). Compared with sham and control groups, the number of vGluT1 and vGluT3 positive neurons in VaD rats decreased in hippocampal CA1-3 region, and the number of vAChT positive neurons in hippocampal CA1-3 was also signifcantly decreased (P〈0.01). Conclusion: Glutamate, cholinergic vesicle cargo function defects, glutamate, central cholinergic neurotransmitter imbalance, neuronal loss, CA1-CA3 hippocampus information loop destruction is the main cause of cognitive dysfunction in rats under the ischemic conditions.
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