ATP敏感性K^+通道在海马缺氧损伤中的作用  

Role of ATP-sensitive Potassium Channels in Anoxia-induced Neuronal Injury of Rat Hippocampus

作　　者：万勤[1] 要航[1] 刘振伟[1] 丁爱石[1] 王福庄[1] 

机构地区：[1]军事医学科学院基础医学研究所,北京100850

出　　处：《中国神经免疫学和神经病学杂志》1998年第3期129-133,共5页Chinese Journal of Neuroimmunology and Neurology

基　　金：国家自然科学基金!39470278;中国科学院上海生理研究所低氧生理开放实验室资助!875005

摘　　要：目的研究ATP敏感性K+通道阻断剂glipizide（GLI）对缺氧后海马脑片损伤以及海马神经元[Ca(2+)]i变化的影响。方法以大鼠离体海马脑片和体外分散培养的海马神经元为标本，分别采用电生理微电极记录技术以及激光扫描共聚焦显微镜监测神经元[Ca(2+)]i的方法。结果预先用GLI（20μmol／L）灌流的海马脑片缺氧后PV持续时间较对照组显著缩短，提示其加重了海马不可逆缺氧损伤的发生；另外急性缺氧可诱导海马神经元[Ca(2+)]i迅速升高，而预先加入GLI（20μmol／L）能显著加剧[Ca(2+)]i的升高程度。结论ATP敏感性K+通道在缺氧过程中的开放对大鼠海马脑区具有重要的保护作用，它可显著降低缺氧所致神经元[Ca(2+)]i升高，提高海马脑片的抗缺氧能力。这可能是其对抗海马缺氧损伤的主要作用机制之一。To investigate the effects of ATP-sensitive potassium channel blocker,glipizide (GLI), on rat hippocampal slices and cultured hippocampal neuronal [Ca(2+)] i during anoxia; Methods Rat hippocampal slices and cultured hippocampal neurons were studied by means of electrical microelectrode recording technique and confocal laser scanning microscope, respectively. Results The PV sustained time of hippocampal slices pretreated with GLI (20umol/L) after anoxia was markedly shorter than that of control, suggesting that the irreversible Injury in hippocampus evoked by anoxia were delayed. On the other hand, acute anoxia induced a rapid increase of [Ca(2+)] i in hippocampal neurons and this could be significantly aggravated by 20umol/L GLI. Conclusion The opening of ATP-sensitive potassium channels during anoxia play an important protective role against the anoxic injury in rat hippocampus, which may be related to its inhibitory effect on neuronal [Ca2+] i elevation and consequently increased endurance against anoxia.

关 键 词：ATP 敏感性K^+通道 缺氧 海马 损伤 

分 类 号：R364[医药卫生—病理学]