Tagaya M, Matsuyama T, Nakamura H, Hata R, Shimizu S, Kiyama H, Matsumoto M, Sugita M
Fifth Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
J Cereb Blood Flow Metab. 1995 Nov;15(6):1132-6. doi: 10.1038/jcbfm.1995.140.
To assess whether ischemia could induce GAP-43 mRNA expression, we performed in situ hybridization in gerbil brains that had been subjected to 5 min of global ischemia. In control dentate granule cells, little hybridization was detected in contrast to the intense signal generated by pyramidal neurons of the adult hippocampal formation. After ischemia, we detected a robust GAP-43 signal over hippocampal granule cells at 3 h of reperfusion, persisting through 7 days, and disappearing by 14 days. This demonstrated GAP-43 gene induction after ischemia, and suggests that GAP-43 may be involved in reactive events, including fiber sprouting and synaptic reorganization, that follow ischemia.
为评估局部缺血是否能诱导GAP - 43信使核糖核酸表达,我们对经历了5分钟全脑缺血的沙鼠脑进行了原位杂交。在对照齿状颗粒细胞中,与成年海马结构的锥体神经元产生的强烈信号相比,几乎检测不到杂交信号。局部缺血后,在再灌注3小时时,我们在海马颗粒细胞上检测到强烈的GAP - 43信号,该信号持续7天,到14天时消失。这证明了局部缺血后GAP - 43基因的诱导,并表明GAP - 43可能参与了局部缺血后的反应性事件,包括纤维发芽和突触重组。