Ocorr K A, Schulman H
Department of Pharmacology, Stanford University School of Medicine, California 94305.
Neuron. 1991 Jun;6(6):907-14. doi: 10.1016/0896-6273(91)90231-n.
In vitro phosphorylation of multifunctional Ca2+/calmodulin-dependent protein kinase (CaM kinase) converts it to a form that is independent of Ca2+. We demonstrate that significant Ca(2+)-independent CaM kinase activity is present in untreated hippocampal slices. Two manipulations that produce a long-lasting enhancement of neuronal activity in hippocampal slices, elevated extracellular Ca2+ or depolarization with high K+, generate additional Ca(2+)-independent activity. This increase is dependent on extracellular Ca2+ and is correlated with an increased phosphorylation of CaM kinase. In contrast, CaM kinase in posterior pituitary, a brain structure that is not thought to be involved in memory-related processes, is not modulated by depolarization. These results suggest that the Ca(2+)-independent form of CaM kinase may modulate neuronal activity in the hippocampus.
多功能钙调蛋白依赖性蛋白激酶(CaM激酶)的体外磷酸化将其转化为一种不依赖于钙离子的形式。我们证明,未经处理的海马切片中存在显著的不依赖钙离子的CaM激酶活性。两种能使海马切片中神经元活动产生持久增强的操作,即细胞外钙离子浓度升高或用高钾去极化,会产生额外的不依赖钙离子的活性。这种增加依赖于细胞外钙离子,并且与CaM激酶磷酸化增加相关。相比之下,垂体后叶中的CaM激酶,一种被认为不参与记忆相关过程的脑结构,不会被去极化所调节。这些结果表明,不依赖钙离子形式的CaM激酶可能调节海马体中的神经元活动。