首都医科大学学报 ›› 2006, Vol. 27 ›› Issue (3): 355-357.

• 临床研究 • 上一篇    下一篇

自发性2型糖尿病小鼠脑组织胆碱能神经递质系统的研究

王宪玲1, 贾建平1, 左萍萍2, 杨楠2   

  1. 1. 首都医科大学宣武医院神经内科;2. 协和医科大学基础医学研究所药理室
  • 收稿日期:2005-07-29 修回日期:1900-01-01 出版日期:2006-06-24 发布日期:2006-06-24

Study on the Acetylcholine System in the Brain of Non-Insulin-Dependent Diabetes Mellitus Animal Model, KK-Ay Mice

Wang Xianling1, Jia Jianping1, Zuo Pingping2, Yang Nan2   

  1. 1. Neurology Department, Xuanwu Hospital, Capital University of Medical Sciences;2. Pharmacy Department of Peking Union Medical College
  • Received:2005-07-29 Revised:1900-01-01 Online:2006-06-24 Published:2006-06-24

摘要:

目的 探讨糖尿病脑病的发病机制.方法应用一种自发性2型糖尿病动物模型,研究其发病早期行为学和脑组织形态学的变化,以及胆碱能神经递质及其受体与糖尿病脑病的关系.结果糖尿病小鼠发病早期出现认知功能障碍和脑组织形态学改变;糖尿病小鼠发病6周时,脑皮质和海马组织的胆碱乙酰转移酶(choline acetyltransferase,ChAT)活性与正常对照组比较无明显改变(P>0.05).发病12周时皮质组织的ChAT活性较正常对照组降低了39%(P<0.05),海马组织下降了36%(P<0.05);糖尿病动物模型KK-Ay小鼠发病6周和12周时皮质和海马组织的胆碱毒蕈碱受体(M受体)结合于3H-QNB的活性与正常对照比较差异均无统计学意义(P>0.05);结论胆碱能神经递质传递异常在糖尿病脑病发病机制中发挥重要作用.

关键词: 糖尿病脑病, 胆碱乙酰转移酶, 胆碱毒蕈碱受体

Abstract:

Objective To investigate the pathogenetic mechanism of diabetic encephalopathy..Methods The non-insulin-dependent diabetes mellitus (NIDDM) animal models, KK-Ay mice, were used. Their cognitive performance and brain structure were studied. The activity of choline acetyltransferase (ChAT) was assayed with 3 H-CoA as the substrate and the binding activity of radiolabelled 3 H-QNB for acetylcholine muscarinic receptors (Mreceptors) was investigated in the cerebral cortex and hippocampus of KK-Ay mice..Results Cognitive impairment and changes of brain structure of NIDDM mice were found. In the cerebral cortex and hippocampus of KK-Ay mice, the activity of choline acetyltransferase (ChAT) was significantly reduced at 12 weeks of duration compared with that of age-matched controls. The binding activity of 3 H-QNB for M receptor in the diabetic mice was not significantly different from that of the controls..Conclusion The acetylcholine system deficits are closely related to the cognitive impairment of diabetic mice.

Key words: diabetic encephalopathy, choline acetyltransferase(ChAT), M receptor

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