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首页> 外文期刊>The European Journal of Neuroscience >Kv3 K channels enable burst output in rat cerebellar Purkinje cells.
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Kv3 K channels enable burst output in rat cerebellar Purkinje cells.

机译：Kv3 K通道可在大鼠小脑浦肯野细胞中产生突发输出。

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Abstract The ability of cells to generate an appropriate spike output depends on a balance between membrane depolarizations and the repolarizing actions of K(+) currents. The high-voltage-activated Kv3 class of K(+) channels repolarizes Na(+) spikes to maintain high frequencies of discharge. However, little is known of the ability for these K(+) channels to shape Ca(2+) spike discharge or their ability to regulate Ca(2+) spike-dependent burst output. Here we identify the role of Kv3 K(+) channels in the regulation of Na(+) and Ca(2+) spike discharge, as well as burst output, using somatic and dendritic recordings in rat cerebellar Purkinje cells. Kv3 currents pharmacologically isolated in outside-out somatic membrane patches accounted for approximately 40% of the total K(+) current, were very fast and high voltage activating, and required more than 1 s to fully inactivate. Kv3 currents were differentiated from other tetraethylammonium-sensitive currents to establish their role in Purkinje cells under physiological conditions with current-clamp recordings. Dual somatic-dendritic recordings indicated that Kv3 channels repolarize Na(+) and Ca(2+) spikes, enabling high-frequency discharge for both types of cell output. We further show that during burst output Kv3 channels act together with large-conductance Ca(2+)-activated K(+) channels to ensure an effective coupling between Ca(2+) and Na(+) spike discharge by preventing Na(+) spike inactivation. By contributing significantly to the repolarization of Na(+) and especially Ca(2+) spikes, our data reveal a novel function for Kv3 K(+) channels in the maintenance of high-frequency burst output for cerebellar Purkinje cells.
机译：摘要细胞产生适当的尖峰输出的能力取决于膜去极化与K（+）电流的再极化作用之间的平衡。 K（+）通道的高压激活Kv3类使Na（+）尖峰重新极化，以维持高频放电。但是，对于这些K（+）通道塑造Ca（2+）尖峰放电的能力或调节Ca（2+）尖峰依赖的突发输出的能力知之甚少。在这里，我们使用大鼠小脑浦肯野细胞的体细胞和树突状记录，确定Kv3 K（+）通道在Na（+）和Ca（2+）尖峰放电以及突发输出的调节中的作用。药理学上分离出来的Kv3电流约占总K（+）电流的40％，非常快且高电压激活，并且需要1秒钟以上的时间才能完全失活。将Kv3电流与其他四乙基铵敏感电流区分开，以在具有电流钳记录的生理条件下确定其在Purkinje细胞中的作用。双重体细胞树突状记录表明，Kv3通道使Na（+）和Ca（2+）尖峰重新极化，从而使两种类型的电池输出都可以进行高频放电。我们进一步表明，在突发输出期间，Kv3通道与大电导Ca（2+）激活的K（+）通道一起起作用，以通过防止Na（+）来确保Ca（2+）和Na（+）尖峰放电之间的有效耦合。 ）峰值失活。通过极大地促进Na（+）尤其是Ca（2+）尖峰的复极化，我们的数据揭示了Kv3 K（+）通道在维持小脑浦肯野细胞高频突波输出中的新功能。

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