海马脑片缺氧损伤电位机制的研究  

MECHANISMS OF HYPOXIC INJURYPOTENTIAL IN HIPPOCAMPALSLICES

作　　者：唐建民[1] 刘振伟[1] 丁爱石[1] 王福庄[1] 

机构地区：[1]北京军事医学科学院基础医学研究所,大庆职工医学院病理生理教研室

出　　处：《中国应用生理学杂志》1996年第2期165-169,共5页Chinese Journal of Applied Physiology

基　　金：国家自然科学基金;中国科学院低氧生理开放实验室资助

摘　　要：本实验在海马脑片采用微电极记录技术，观察了缺氧损伤电位（ＨＩＰ）的电生理特性，并研究了其产生机制。实验结果表明：①ＨＩＰ是突触在缺氧过程中功能暂时恢复的反应；②随着缺氧程度的加重，ＨＩＰ出现时间前移，持续时间缩短；③ＨＩＰ的出现表明突触功能的丧失发生在突触膜损伤之前，其消失代表突触传递不可逆性损伤的发生，即突触膜损伤的开始；④大剂量腺苷不能阻止ＨＩＰ的产生，表明ＨＩＰ的出现不是由于腺苷浓度的降低。Electrical properties and mechanisms of hypoxic injury potential(HIP)were studied in areaCA1 pyramidaI neurons from rat hippocampal slices by means of microelectrode technique,Theresults indicated that(1)HIP was a transient recovery of synaptic function during hypoxia;(2)HIP occurred earlier and its duration was shortened when hypoxia was aggravated;(3)thesynaptic membrane was not damaged by hypoxia untiI HIP disappeared;(4) high dose ofadenosine failed to block the appearance of HIP,indicating that the reduction of adenosine didnot account for the appearance of HIP.

关 键 词：海马脑片 缺氧 缺氧损伤电位 腺苷 

分 类 号：R741.02[医药卫生—神经病学与精神病学] R594.302[医药卫生—临床医学]