A role for gamma-aminobutyric acid (GABA) in the evolution of delayed neuronal death following ischemia.
A role for gamma-aminobutyric acid (GABA) in the evolution of delayed neuronal death following ischemia.
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γ-氨基丁酸（GABA）在缺血后迟发性神经元死亡进化中的作用。
DOI：
10.1007/bf00999539
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发表时间：
1988
影响因子：
3.6
通讯作者：
Sternau,LL
中科院分区：
文献类型：
--
作者：
Lust,WD;Assaf,HM;Ricci,AJ;Ratcheson,RA;Sternau,LL
在沙土鼠双侧脑缺血5min后的第4天，检测一系列可能的神经保护剂对防止海马区CA1神经元丢失的效果。与GABA能系统相关的药物被确定为最有效的药物，但只有在缺血发作之前给药，这表明在缺血期间存在γ-氨基丁酸相关事件，触发这些细胞的迟发性神经元死亡。在模拟缺氧和/或缺血的条件下，测定了沙土鼠海马片中GABA和谷氨酸的单向释放。戊巴比妥是GABA能药中最有效的一种，对谷氨酸的时间依赖性释放几乎没有影响。相反，戊巴比妥在缺氧和缺血时都减少了GABA的释放，但只在孵育25到30分钟后才减少。
A series of putative neuroprotective agents was tested to determine their efficacy in preventing the loss of the CA 1 neurons of the hippocampus at 4 days following 5 min of bilateral ischemia in the gerbil. Agents associated with the GABAergic system were determined to be the most effective, but only when given prior to the ischemic episode, suggesting that there was aγ-aminobutyric acid (GABA)-related event during ischemia which triggers the delayed neuronal death of these cells. In this report, the unidirectional release of GABA and glutamate from gerbil hippocampal slices was determined under conditions mimicking anoxia and/or ischemia. Pentobarbital, the most effective of the GABAergic agents, had little or no effect on the time-dependent release of glutamate. In contrast, pentobarbital reduced in release of GABA in both anoxia and ischemia, but only after 25 to 30 min of incubation.