Mechanisms of potentiation by calcium-calmodulin kinase II of postsynaptic sensitivity in rat hippocampal CA1 neurons.
Mechanisms of potentiation by calcium-calmodulin kinase II of postsynaptic sensitivity in rat hippocampal CA1 neurons.
复制标题
钙-钙调蛋白激酶 II 增强大鼠海马 CA1 神经元突触后敏感性的机制。
DOI：
10.1152/jn.1997.78.5.2682
复制
发表时间：
1997
影响因子：
2.5
通讯作者：
Malinow,R
中科院分区：
文献类型：
--
作者：
Shirke,AM;Malinow,R
作者：Aneil M.和Roberto Malinow.大鼠海马CA 1神经元中突触后敏感性的钙-钙调蛋白激酶II增强作用的机制.神经生理学杂志78：2682-2692，1997.将预先激活的重组α-钙-钙调素依赖性多功能蛋白激酶Ⅱ（CaMK Ⅱ）灌流到海马脑片CA 1区神经元内，以检测其对突触传递的影响和对外源性谷氨酸类似物的反应。在测量基线传输后，CaMKII* 的内部灌注增加了大鼠海马神经元的突触强度，并减少了突触失败的分数。在测量对所施加的发射器的基线响应后，CaMK II * 灌注增强对红藻氨酸的响应，但不增强对N-甲基-d-天冬氨酸的响应。CaMKII* 的内部灌注增强了红藻氨酸盐的最大作用。增强由CaMKII * 没有改变的时间过程中的响应红藻氨酸，而增加响应的大小，通过操纵脱敏或失活速率常数显着改变的时间过程中的响应。非平稳波动分析红藻氨酸盐的反应表明，由CaMKII* 增强后的变异系数下降。这些数据支持CaMK II通过增加活性α-氨基-3-羟基-5-甲基异恶唑-4-丙酸/红藻氨酸通道的可用数量来增加突触后反应性的假设，并表明在长时程增强的表达期间可能发生类似的过程。
Shirke, Aneil M. and Roberto Malinow.Mechanisms of potentiation by calcium-calmodulin kinase II of postsynaptic sensitivity in rat hippocampal CA1 neurons.J. Neurophysiol.78: 2682–2692, 1997. Preactivated recombinant α-calcium–calmodulin dependent multifunctional protein kinase II (CaMKII*) was perfused internally into CA1 hippocampal slice neurons to test the effect on synaptic transmission and responses to exogenous application of glutamate analogues. After measurement of baseline transmission, internal perfusion of CaMKII* increased synaptic strength in rat hippocampal neurons and diminished the fraction of synaptic failures. After measurement of baseline responses to applied transmitter, CaMKII* perfusion potentiated responses to kainate but not responses toN-methyl-d-aspartate. Internal perfusion of CaMKII*potentiated the maximal effect of kainate. Potentiation byCaMKII* did not change the time course of responses to kainate, whereas increasing response size by pharmacologically manipulating desensitization or deactivation rate constants significantly altered the time course of responses. Nonstationary fluctuation analysis of responses to kainate showed a decrease in the coefficient of variation after potentiation by CaMKII*. These data support the hypothesis that CaMKII increases postsynaptic responsiveness by increasing the available number of active α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate channels and suggests that a similar process may occur during the expression of long-term potentiation.