Protein kinase C activation decreases activity-dependent attenuation of dendritic Na+ current in hippocampal CA1 pyramidal neurons
Protein kinase C activation decreases activity-dependent attenuation of dendritic Na+ current in hippocampal CA1 pyramidal neurons
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DOI：
10.1152/jn.1998.79.1.491
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发表时间：
1998-01-01
影响因子：
2.5
通讯作者：
Johnston, D
中科院分区：
文献类型：
--
作者：
Colbert, CM;Johnston, D
蛋白激酶C激活降低海马CAl锥体神经元树突Na+电流的活性依赖性衰减。中国生物医学工程学报，32(3):491-495,1998。在重复放电过程中，从CAl锥体神经元体记录的动作电位在振幅上保持相对一致。相反，在突波序列中，树突中反向传播动作电位的振幅逐渐减小。这种与活动相关的振幅下降取决于在训练期间的发射频率和与体细胞的距离。之前，我们描述了Na+通道的一个特性，该特性为树突动作电位振幅的活性依赖性提供了一个合理的机制：在动作电位序列中，通过失活（与快速失活不同），可用Na+电流减少，失活在开始时看起来很快，但恢复缓慢且依赖于电压。在这项研究中，我们发现phorbol酯激活蛋白激酶C可以降低细胞附着的树突斑块中药理学分离的Na+电流的活性依赖性失活，而不是体细胞斑块。同样，在全细胞记录中，佛波酯降低了训练期间反向传播的树突动作电位的衰减。这些结果表明了蛋白激酶C对树突Na+通道的新作用，并进一步支持了树突动作电位的活性依赖性来源于Na+通道的失活特性的假设。
Protein kinase C activation decreases activity-dependent attenuation of dendritic Na+ current in hippocampal CAl pyramidal neurons. J. Neurophysiol. 79: 491-495, 1998. Action potentials recorded from the soma of CAl pyramidal neurons remain relatively uniform in amplitude during repetitive firing. In contrast, the amplitudes of back-propagating action potentials in dendrites decrease progressively during a spike train. This activity-dependent decrease in amplitude is dependent on the frequency of firing during the train and distance from the soma. Previously, we described a property of Na+ channels that provides a plausible mechanism for the activity dependence of the amplitude of the dendritic action potentials: available Na+ current decreases during trains of action potentials through an inactivation, distinct from fast inactivation, that appears rapid in onset, but slow and voltage-dependent in its recovery. In this study we found that activation of protein kinase C by phorbol esters decreased this activity-dependent inactivation of pharmacologically isolated Na+ current in cell-attached dendritic, but not somatic, patches. Similarly in whole cell recordings phorbol esters decreased the attenuation of back-propagating dendritic action potentials during trains. These results indicate a novel effect of protein kinase C on the dendritic Na+ channel and further support the hypothesis that the activity dependence of the dendritic action potentials is derived from the inactivation properties of Na+ channels.