Ishimaru H, Takahashi A, Ikarashi Y, Maruyama Y
Department of Neuropsychopharmacology (Tsumura), Gunma University School of Medicine, Japan.
Brain Res. 1995 Feb 27;673(1):112-8. doi: 10.1016/0006-8993(94)01409-b.
Effects of pentobarbital on the release of acetylcholine (ACh), the area of CA1 pyramidal cell soma and the immunoreactivity of choline acetyltransferase (ChAT) in the hippocampus following ischemia were investigated. Five minute ischemia significantly decreased the KCl-, atropine-induced and basal release of ACh and the area of CA1 pyramidal cell soma in the hippocampus. Moreover, ChAT immunoreactivity, a marker of pre-synaptic terminal survival in the cholinergic neurons, was lowered 14 days after ischemia-recirculation. Although treatment with pentobarbital (50 mg/kg) 30 min before ischemia provided complete protection against hippocampal CA1 pyramidal cell death, pentobarbital failed to improve the decrements of ACh release and the low ChAT immunoreactivity over the test period. Our study thus showed discrepancies between pre-synaptic neurochemical estimation and post-synaptic morphological observation of the effect of pentobarbital on ischemic damage.
研究了戊巴比妥对缺血后海马中乙酰胆碱（ACh）释放、CA1锥体细胞体面积以及胆碱乙酰转移酶（ChAT）免疫反应性的影响。五分钟的缺血显著降低了海马中氯化钾、阿托品诱导的以及基础状态下的ACh释放，以及CA1锥体细胞体面积。此外，作为胆碱能神经元突触前终末存活标志物的ChAT免疫反应性在缺血再灌注14天后降低。尽管在缺血前30分钟给予戊巴比妥（50mg/kg）可完全保护海马CA1锥体细胞免于死亡，但在测试期间戊巴比妥未能改善ACh释放的减少和低ChAT免疫反应性。因此，我们的研究显示了戊巴比妥对缺血性损伤影响的突触前神经化学评估与突触后形态学观察之间的差异。
