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GABA 是海马主要抑制性神经递质。实验性脑缺血再灌流后海马 GABA 发生急剧升高,又显著降低于正常的双相改变;再灌流后海马 CA1区持续兴奋性增高、返回抑制减弱,齿状回和 CA3区却是兴奋性减低、返回抑制增强;若事先给一定剂量 GABA 能模拟剂能完全或部分保护 CA1区不受缺血损害;因而推测 GABA 改变、海马内原性抑制降低致兴奋—抑制失衡,可能是脑缺血再灌流后海马迟发性神经元损害的因素之一。
GABA is a major inhibitory neurotransmitter in the hippocampus. The hippocampus GABA increased sharply after experimental cerebral ischemia-reperfusion and was significantly lower than the normal biphasic changes. After reperfusion, the hippocampal CA1 area continued to increase excitability, and the return inhibition decreased. The dentate gyrus and CA3 area were excitatory Reduce, return inhibition increased; if given a dose of GABA simulant can be completely or partially protected CA1 area from ischemic damage; presumably GABA changes in the hippocampus caused by reduced inhibition of intrinsic excitability - inhibition of imbalance may be cerebral ischemia One of the factors of delayed neuronal damage in the hippocampus after perfusion.