Sims N R, Heward S L
Department of Medical Biochemistry, Flinders University, Adelaide, Australia.
Brain Res. 1994 Oct 31;662(1-2):216-22. doi: 10.1016/0006-8993(94)90815-x.
This study examined the effect of 1,3-butanediol on the selective loss of CA1 pyramidal neurons following a short period of near-complete forebrain ischemia. Injection of 55 mmol 1,3-butanediol/kg body weight at 24 h of recirculation and again at 36 h following 10 min of forebrain ischemia markedly reduced damage to CA1 neurons examined at 72 h of recirculation compared with that in saline-treated rats. Comparable treatment with ethanol did not cause significant protection. Neuronal loss was also not reduced by 1,3-butanediol treatment when the ischemic period was extended to 15 min or by single treatments at 24 h or 36 h following 10 min of ischemia. However, a single treatment 5 min after reversal of 10 min of ischemia was effective in ameliorating cell loss. The difference in effectiveness of 1,3-butanediol following 10 min and 15 min of ischemia is consistent with a number of previous studies, indicating that the processes leading to loss of CA1 neurons are modified when the ischemic period is extended. Previous findings that 1,3-butanediol reduced damage in other ischemia-susceptible neuronal subpopulations but not in CA1 neurons most likely reflected the longer period of ischemia which was used. The results of the present investigation demonstrate that administration of 1,3-butanediol offers a novel approach for interfering with post-ischemic loss of CA1 neurons following a brief ischemic period which is effective even when initiated after prolonged recirculation periods.
本研究检测了1,3 - 丁二醇对短时间近乎完全性前脑缺血后CA1锥体神经元选择性丢失的影响。在前脑缺血10分钟后再灌注24小时时注射55 mmol 1,3 - 丁二醇/千克体重，并在36小时时再次注射，与生理盐水处理的大鼠相比，在再灌注72小时时检测发现，这显著减少了CA1神经元的损伤。用乙醇进行类似处理未产生显著的保护作用。当缺血时间延长至15分钟时，或在缺血10分钟后的24小时或36小时进行单次处理时，1,3 - 丁二醇处理也未减少神经元丢失。然而，在10分钟缺血逆转后5分钟进行单次处理可有效减轻细胞丢失。1,3 - 丁二醇在10分钟和15分钟缺血后的有效性差异与之前的多项研究一致，表明当缺血时间延长时，导致CA1神经元丢失的过程会发生改变。先前的研究发现1,3 - 丁二醇可减少其他易受缺血影响的神经元亚群的损伤，但对CA1神经元无效，这很可能反映了所使用的缺血时间更长。本研究结果表明，给予1,3 - 丁二醇为干预短暂缺血期后CA1神经元的缺血后丢失提供了一种新方法，即使在长时间再灌注期后开始使用也有效。
