谷氨酸的
加巴能
神经科学
海马结构
海马体
神经化学
神经传递
脑病
谷氨酸受体
谷氨酸脱羧酶
神经元
医学
生物
内科学
抑制性突触后电位
受体
生物化学
酶
作者
Chun Wang,Juan Li,S. J. Zhao,Li Huang
出处
期刊:Brain Research
[Elsevier BV]
日期:2020-09-01
卷期号:1742: 146863-146863
被引量:10
标识
DOI:10.1016/j.brainres.2020.146863
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI