摘要
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。
In order to elucidate the relation between hippocampal GABA、AchE,and delayed neuronal damage(DND),GABA content and AchE activity of the hippocampal subfields after cerebral ischemia/reperfusion were analyzed.The hippocampal pathologic changes were also observed.It was found :During 5 min reperfusion, the hippocampal sub fields GABA content elevated significantly.During 1h and 6～12h reperfusion, theGABA content reduced obviously,the CA_1 area being more obvious.During 5～1h re-perfusion,the AchE activity of hippocampal subfields was increased markedly.After 48hreperfusion,the ischemic change of the hippocampal CA_1 appeared.These results suggested:(1)After reperfusion,the GABA content decreased or the hippocampal intrinsic inhibi-tion reduced might be one of the factors in DND.(2)Early stage after reperfusion,theelevation of AchE activity reflects the metabolic change of Ach.This change may relateto DND.(3)After reperfusion,the hippocampal CA_1 vulnerability is not only relaed tothe neurotransmitter changes,but the biochemical and physiological nature of the CA_1neurons also played an important role.
出处
《中国病理生理杂志》
CSCD
北大核心
1994年第4期434-438,共5页
Chinese Journal of Pathophysiology
关键词
脑缺血
海马
氨基丁酸
神经元损伤
Cerebral ischemia
Hippocampus
γ-aminobutyric acid
Acetylcholinesterase
