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Kv1通道选择性地预防大鼠浦肯野细胞中的树突状超兴奋性。

Kv1 channels selectively prevent dendritic hyperexcitability in rat Purkinje cells.

作者信息

Khavandgar Simin, Walter Joy T, Sageser Kristin, Khodakhah Kamran

机构信息

Department of Neuroscience, Albert Einstein College of Medicine, 506 Kennedy Center, 1410 Pelham Parkway South, Bronx, NY 10461, USA.

出版信息

J Physiol. 2005 Dec 1;569(Pt 2):545-57. doi: 10.1113/jphysiol.2005.098053. Epub 2005 Oct 6.

Abstract

Purkinje cells, the sole output of the cerebellar cortex, encode the timing signals required for motor coordination in their firing rate and activity pattern. Dendrites of Purkinje cells express a high density of P/Q-type voltage-gated calcium channels and fire dendritic calcium spikes. Here we show that dendritic subthreshold Kv1.2 subunit-containing Kv1 potassium channels prevent generation of random spontaneous calcium spikes. With Kv1 channels blocked, dendritic calcium spikes drive bursts of somatic sodium spikes and prevent the cell from faithfully encoding motor timing signals. The selective dendritic function of Kv1 channels in Purkinje cells allows them to effectively suppress dendritic hyperexcitability without hindering the generation of somatic action potentials. Further, we show that Kv1 channels also contribute to dendritic integration of parallel fibre synaptic input. Kv1 channels are often targeted to soma and axon and the data presented support a major dendritic function for these channels.

摘要

浦肯野细胞是小脑皮质的唯一输出神经元,其放电频率和活动模式编码了运动协调所需的时间信号。浦肯野细胞的树突表达高密度的P/Q型电压门控钙通道,并产生树突钙峰电位。我们在此表明,含有Kv1.2亚基的树突阈下Kv1钾通道可防止随机自发钙峰电位的产生。当Kv1通道被阻断时,树突钙峰电位驱动胞体钠峰电位的爆发,并阻止细胞忠实地编码运动时间信号。浦肯野细胞中Kv1通道的选择性树突功能使其能够有效抑制树突过度兴奋,而不妨碍胞体动作电位的产生。此外,我们表明Kv1通道也有助于平行纤维突触输入的树突整合。Kv1通道通常定位于胞体和轴突,本文提供的数据支持这些通道具有主要的树突功能。

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