摘要
目的:探讨脑缺血诱导小鼠大脑皮层γ-氨基丁酸(GABA)能神经元电生理特性的变化。方法:取生后15~17d的FVB-Tg(GADGFP)4570Swn/J小鼠大脑做冠状切片(400μm),采用IR-DIC显微镜选择大脑皮层GA-BA能神经元,运用Axoclamp-2B放大器全细胞记录模式记录大脑皮层GABA能神经元动作电位的阈电位(Vts)和绝对不应期(ARP),分析群集发放的动作电位间距(ISI)和动作电位峰时程标准差(SDST)。结果:与缺血前相比,缺血后大脑皮层GABA能神经元产生群集动作电位的ISI和SDST降低(P<0.01),Vts和ARP延长(P<0.01)。结论:缺血改变导致GABA能神经元动作电位的不应期和阈电位升高,使大脑皮层GABA能神经元兴奋性降低,动作电位的编码能力降低。
Aim : To study the changes of the electrophysiological properties of cortical Gamma aminobutyric acidergic (GABAergic) neurons induced by ischemia. Methods:The tissue blocks of cerebral cortex of GFP mice aged 15 - 17 d were quickly isolated, and the cortical slices (400 μm) were cut. Cortical GABAergic neurons labeled with GFP were selected under IR-DIC/fluorescent microscope. The threshold potentials (Vts) for firing spikes and absolute refractory periods (ARP) subsequent to each spike were recorded in whole-cell model using an Axoclamp-2B amplifier; and electrical signals were inputed into pClamp 9.2 for data acquisition and analysis of inter-spike interval(ISI) and standard deviation of spike timing(SDST). Results: Compared with those before ischemia, ARP and Vts prolonged (P 〈 0. 01 ), and ISI and SDST decreased(P 〈0.01 ). Conclusion: The ischemia promotes ARP and Vts of sequential spikes and reduces the excitation and deteriorates spike encoding of GABAergie neuron.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2009年第4期758-760,共3页
Journal of Zhengzhou University(Medical Sciences)
基金
安徽省教育厅青年人才基金资助项目2008JQ1104