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为探讨海马ＧＡＢＡ、ＡｃｈＥ和迟发性神经元损害（ｄｅｌａｙｅｄｎｅｕｒｏｎａｌｄａｍａｇｅ，ＤＮＤ）的关系，观察了脑缺血／再灌注后大鼠海马亚区ＧＡＢＡ含量、ＡｃｈＥ活性和海马组织病理改变。发现再灌注５ｍｉｎ，海马亚区ＧＡＢＡ含量显著升高，再灌注１ｈ和６～１２ｈ，ＧＡＢＡ含量明显降低，ＣＡ＿１区更明显。再灌注５ｍｉｎ至１ｈ，海马亚区ＡｃｈＥ活性明显升高。再灌注４８ｈ后，光镜下见海马ＣＡ＿１区神经元出现缺血性改变，提示：（１）再灌注后，ＧＡＢＡ含量减少、海马内源性抑制降低可能是ＣＡ＿１区ＤＮＤ的因素之一。（２）再灌注早期ＡｃｈＥ活性升高，提示Ａｃｈ代谢变化可能和ＤＮＤ有关。（３）再灌注后ＧＡＢＡ和ＡｃｈＥ在海马各亚区的明显改变，提示ＣＡ＿１区选择性易损和递质代谢变化密切相关，而ＣＡ＿１区神经元本身的生理生化特性也起着重要的作用。
To investigate the relationship between GABA, AchE and delayed neuronal damage (DND) in hippocampus, the levels of GABA and AchE in hippocampal subfields and the histopathological changes of hippocampus were observed after cerebral ischemia / reperfusion in rats. It was found that GABA content in hippocampus subregion increased significantly 5 min after reperfusion, and the content of GABA decreased significantly at 1h and 6 ~ 12h after reperfusion. Reperfusion 5min to 1h, Hippocampal subregion AchE activity was significantly increased. 48h after reperfusion, ischemic changes of neurons in hippocampal CA1 area were observed under light microscope, which indicated that: (1) After reperfusion, the decrease of GABA content and the decrease of endogenous inhibition of hippocampus may be one of the factors of DND in CA1 area. (2) The activity of AchE increased in the early stage of reperfusion, suggesting that the changes of Ach metabolism may be related to DND. (3) The obvious changes of GABA and AchE in hippocampus subregion after reperfusion suggest that the selective vulnerability and the changes of neurotransmitter metabolism are closely related in CA 1 area, while the physiological and biochemical characteristics of CA 1 area neurons also play an important role.