Onodera H, Yamasaki Y, Kogure K, Miyamoto E
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Brain Res. 1995 Jun 26;684(1):95-8. doi: 10.1016/0006-8993(95)00382-z.
Calcium/calmodulin-dependent protein kinase II (kinase II) and protein phosphatase 2B (calcineurin) immunoreactivity in the rat hippocampus was studied 100 days after ischemic damage to hippocampal CA1 pyramidal neurons. One-hundred days after ischemia, only a few CA1 pyramidal neurons survived and they exhibited enhanced kinase II and calcineurin immunoreactivity in their basal and apical dendrites. The stratum lucidum of the CA3 (mossy fiber terminal area) had enhanced kinase II and calcineurin immunoreactivity. These results suggest activity-dependent regulation and redistribution of kinase II and calcineurin after intervention in neuronal circuitry.
在海马CA1锥体神经元发生缺血性损伤100天后,对大鼠海马中的钙/钙调蛋白依赖性蛋白激酶II(激酶II)和蛋白磷酸酶2B(钙调神经磷酸酶)免疫反应性进行了研究。缺血100天后,仅少数CA1锥体神经元存活,并且它们在其基底树突和顶树突中表现出增强的激酶II和钙调神经磷酸酶免疫反应性。CA3的透明层(苔藓纤维终末区)具有增强的激酶II和钙调神经磷酸酶免疫反应性。这些结果表明,在对神经元回路进行干预后,激酶II和钙调神经磷酸酶存在活性依赖性调节和重新分布。