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.

中文翻译：

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糖尿病性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。

糖尿病脑病是中枢神经系统 (CNS) 中与糖尿病相关的严重并发症，其特征是神经化学和结构变化受损，导致认知功能障碍。其细胞和分子机制尚不清楚，临床方法仍缺乏有希望的治疗方法。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糖尿病脑病期间不同海马神经元的变化。与对照组的数据相比，糖尿病脑病永久性地损害了 GABA 能神经元的兴奋性和由 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。我们的研究结果强调了海马区糖尿病性脑病期间 GABA 能神经元和谷氨酸能神经元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预防糖尿病性脑病进展功能的策略。