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首页> 外文期刊>Brain research >The role of small-conductance Ca(2+)-activated K(+) channels in the modulation of 4-aminopyridine-induced burst firing in rat cerebellar Purkinje cells.
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The role of small-conductance Ca(2+)-activated K(+) channels in the modulation of 4-aminopyridine-induced burst firing in rat cerebellar Purkinje cells.

机译：小电导Ca（2+）激活K（+）通道在大鼠小脑Purkinje细胞中4-氨基吡啶诱导的猝发放电的调制中的作用。

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摘要

Small-conductance Ca(2+)-activated K(+) channels (SK) regulate the firing properties of many types of neurons. In the mammalian brain, 3 subunits (SK1-SK3) are expressed with different distributions. Purkinje cells (PCs), the central neuron of the cerebellar basic circuit, express the SK2 subunit in their soma and dendrites. Mature PCs fire bursts of Na(+)-Ca(2+) spikes that constitute the sole output of the cerebellar cortex. Application of 4-aminopyridine (4-AP), blocker of Kv potassium channels in brain slices, augments the electrical activity and burst firing in mature PCs. Using conventional intracellular recordings from acutely prepared brain slices, we examined the role of SK channels in regulation of the 4-AP-induced burst activity in PCs. Application of apamin, blocker of the SK channels induced a depolarization in the membrane potential particularly between spontaneous bursts induced by 4-AP. To study the role of SK channels in 4-AP-induced burst, the spontaneous activity was suppressed by injecting adequate hyperpolarizing current and the bursts were evoked by depolarizing pulse. Apamin decreased the duration of the evoked bursts in 4-AP-treated neurons. It also prolonged the duration and repolarization time of the Ca(2+) spikes and decreased the number of and interval between Na(+) spikes in the 4-AP-induced bursts. Decrease in interval between Na(+) spikes was also seen in the rebound responses. Our findings suggest that SK channels are active at membrane potentials close to resting membrane potential in mature PCs and play an important role in the regulation of neuronal hyperexcitability and burst firing.
机译：小电导Ca（2+）激活K（+）通道（SK）调节许多类型神经元的放电特性。在哺乳动物的大脑中，三个亚基（SK1-SK3）以不同的分布表达。小脑基本回路的中枢神经元浦肯野细胞（PC）在其体细胞和树突中表达SK2亚基。成熟的PC发射Na（+）-Ca（2+）尖峰，构成小脑皮层的唯一输出。 4-氨基吡啶（4-AP）是脑切片中Kv钾离子通道的阻滞剂，可增强成熟PC的电活动和爆发放电。使用来自急性准备的脑片的常规细胞内记录，我们检查了SK通道在调节4-AP诱导的PC爆发活动中的作用。磷灰石，SK通道的阻滞剂的应用引起了膜电位的去极化，特别是在由4-AP引起的自发爆发之间。为了研究SK通道在4-AP诱导的猝发中的作用，通过注入足够的超极化电流抑制了自发活动，并通过去极化脉冲诱发了猝发。 Apamin减少了接受4-AP治疗的神经元诱发的爆发的持续时间。它还延长了Ca（2+）尖峰的持续时间和复极化时间，并减少了4-AP诱发的猝发中Na（+）尖峰的数量和间隔。在反弹响应中还可以看到Na（+）峰之间的间隔减小。我们的发现表明，SK通道在接近成熟PC的静息膜电位的膜电位上具有活性，并且在调节神经元过度兴奋和爆发放电中起重要作用。

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