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糖尿病脑病导致小鼠海马谷氨酸能神经元和 GABA 能神经元之间的神经活动失衡。

Diabetic encephalopathy causes the imbalance of neural activities between hippocampal glutamatergic neurons and GABAergic neurons in mice.

机构信息

Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233040, China.

Department of Pathophysiology, Bengbu Medical College, Bengbu, Anhui 233030, China.

出版信息

Brain Res. 2020 Sep 1;1742:146863. doi: 10.1016/j.brainres.2020.146863. Epub 2020 Apr 28.

DOI:10.1016/j.brainres.2020.146863
PMID:32360099
Abstract

Diabetic encephalopathy is a severe diabetes-related complication in the central nervous system (CNS) that is characterized by the impairment of neurochemical and structural changes leading to cognitive dysfunction. Its cellular and molecular mechanisms are still unclear and clinical approaches are still lacking of promising therapies. In this study, we have investigated the changes of different hippocampal neurons during diabetic encephalopathy in mouse models of diabetes by simultaneously analyzing the activities and synaptic transmission of glutamatergic neurons and GABAergic neurons in brain slices. Compared with the data from a group of control, diabetic encephalopathy permanently impairs the excitability of GABAergic neurons and synaptic transmission mediated by γ-aminobutyric acid (GABA). However, glutamatergic neurons appear to be more excited. Our findings highlight the critical role of the dysfunction of GABAergic neurons and glutamatergic neurons during diabetic encephalopathy in hippocampus to neural impairment as well as a strategy to prevent the function of progress of diabetic encephalopathy by protecting central neurons.

摘要

糖尿病性脑病是一种严重的与糖尿病相关的中枢神经系统(CNS)并发症,其特征是神经化学和结构变化导致认知功能障碍。其细胞和分子机制尚不清楚,临床方法仍缺乏有前途的治疗方法。在这项研究中,我们通过同时分析脑切片中谷氨酸能神经元和 GABA 能神经元的活动和突触传递,研究了糖尿病小鼠模型中糖尿病性脑病期间不同海马神经元的变化。与一组对照数据相比,糖尿病性脑病永久性损害了 GABA 能神经元的兴奋性和γ-氨基丁酸(GABA)介导的突触传递。然而,谷氨酸能神经元似乎更兴奋。我们的发现强调了 GABA 能神经元和谷氨酸能神经元在海马体中糖尿病性脑病期间的功能障碍对神经损伤的关键作用,以及通过保护中枢神经元来防止糖尿病性脑病功能进展的策略。

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