BK channels control cerebellar Purkinje and Golgi cell rhythmicity in vivo.
BK channels control cerebellar Purkinje and Golgi cell rhythmicity in vivo.
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DOI：
10.1371/journal.pone.0007991
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发表时间：
2009-11-24
期刊：
影响因子：
3.7
通讯作者：
Servais L
中科院分区：
文献类型：
--
作者：
Cheron G;Sausbier M;Sausbier U;Neuhuber W;Ruth P;Dan B;Servais L
钙信号在正常中枢神经系统功能和功能障碍中起着核心作用。由于小脑浦肯野细胞表达钙控制的主要调控元件，并代表小脑皮层的唯一整合输出，因此这些细胞的神经活动和钙介导的膜特性的变化有望为小脑的内在生理学和网络生理学提供重要的见解。我们研究了浦肯野细胞在不表达BK钙活化钾通道的基因工程小鼠和BK药理学失活的野生型小鼠中的电生理行为。我们在浦肯野细胞和高尔基细胞中证实了BK的表达。我们证明了遗传或药理学BK失活导致共济失调和小脑皮层β振荡场电位的出现。这种振荡与浦肯野细胞和高尔基细胞的节律性和同步性增强有关。我们假设浦肯野细胞和高尔基细胞刺突放电的时间编码修饰导致了药理学或遗传诱导的共济失调。
Calcium signaling plays a central role in normal CNS functioning and dysfunction. As cerebellar Purkinje cells express the major regulatory elements of calcium control and represent the sole integrative output of the cerebellar cortex, changes in neural activity- and calcium-mediated membrane properties of these cells are expected to provide important insights into both intrinsic and network physiology of the cerebellum. We studied the electrophysiological behavior of Purkinje cells in genetically engineered alert mice that do not express BK calcium-activated potassium channels and in wild-type mice with pharmacological BK inactivation. We confirmed BK expression in Purkinje cells and also demonstrated it in Golgi cells. We demonstrated that either genetic or pharmacological BK inactivation leads to ataxia and to the emergence of a beta oscillatory field potential in the cerebellar cortex. This oscillation is correlated with enhanced rhythmicity and synchronicity of both Purkinje and Golgi cells. We hypothesize that the temporal coding modification of the spike firing of both Purkinje and Golgi cells leads to the pharmacologically or genetically induced ataxia.
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