Laboratory of Electrophysiology, Université Mons-Hainaut, Mons, Belgium.
PLoS One. 2009 Nov 24;4(11):e7991. doi: 10.1371/journal.pone.0007991.
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.
钙信号在中枢神经系统的正常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节元件，并且是小脑皮层唯一的整合输出，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和网络生理学提供重要的见解。我们研究了在不表达 BK 钙激活钾通道的基因工程警报小鼠中和在野生型小鼠中用药理学 BK 失活的情况下浦肯野细胞的电生理行为。我们证实了 BK 在浦肯野细胞中的表达，并且还在高尔基细胞中证明了它。我们证明，无论是遗传还是药理学 BK 失活都会导致共济失调，并导致小脑皮层中出现β振荡场电位。这种振荡与浦肯野和高尔基细胞的节律性和同步性增强相关。我们假设，两种浦肯野和高尔基细胞的尖峰发射的时间编码修饰导致药理学或遗传诱导的共济失调。
