Servais L, Cheron G
Laboratory of Electrophysiology, Université Mons-Hainaut, Belgium.
Neuroscience. 2005;134(4):1247-59. doi: 10.1016/j.neuroscience.2005.06.001.
Fast (approximately 160 Hz) cerebellar oscillation has been recently described in different models of ataxic mice, such as mice lacking calcium-binding proteins and in a mouse model of Angelman syndrome. Among them, calretinin-calbindin double knockout mice constitute the best model for evaluating fast oscillations in vivo. The cerebellum of these mice may present long-lasting episodes of very strong and stable local field potential oscillation alternating with the normal non-oscillating state. Spontaneous firing of the Purkinje cells in wild type and double knockout mice largely differs. Indeed, the Purkinje cell firing of the oscillating mutant is characterized by an increased rate and rhythmicity and by the emergence of synchronicity along the parallel fiber axis. To better understand the driving role played by these different parameters on fast cerebellar oscillation, we simultaneously recorded Purkinje cells and local field potential during the induction of general anesthesia by ketamine or pentobarbitone. Both drugs significantly increased Purkinje cell rhythmicity in the absence of oscillation, but they did not lead to Purkinje cell synchronization or to the emergence of fast oscillation. During fast oscillation episodes, ketamine abolished Purkinje cell synchronicity and inhibited fast oscillation. In contrast, pentobarbitone facilitated fast oscillation, induced and increased Purkinje cell synchronicity. We propose that fast cerebellar oscillation is due to the synchronous rhythmic firing of Purkinje cell populations and is facilitated by positive feedback whereby the oscillating field further phase-locks recruited Purkinje cells onto the same rhythmic firing pattern.
近期在不同的共济失调小鼠模型中发现了快速（约160赫兹）的小脑振荡，比如缺乏钙结合蛋白的小鼠以及安吉尔曼综合征小鼠模型。其中，钙视网膜蛋白-钙结合蛋白双敲除小鼠是评估体内快速振荡的最佳模型。这些小鼠的小脑可能会出现持续时间较长的非常强烈且稳定的局部场电位振荡，与正常的非振荡状态交替出现。野生型和双敲除小鼠浦肯野细胞的自发放电有很大差异。实际上，振荡突变体的浦肯野细胞放电特征是频率增加、节律性增强以及沿平行纤维轴出现同步性。为了更好地理解这些不同参数在小脑快速振荡中所起的驱动作用，我们在通过氯胺酮或戊巴比妥诱导全身麻醉的过程中，同时记录了浦肯野细胞和局部场电位。两种药物在无振荡的情况下均显著增加了浦肯野细胞的节律性，但它们并未导致浦肯野细胞同步化或快速振荡的出现。在快速振荡发作期间，氯胺酮消除了浦肯野细胞的同步性并抑制了快速振荡。相比之下，戊巴比妥促进了快速振荡，诱导并增加了浦肯野细胞的同步性。我们认为，小脑快速振荡是由于浦肯野细胞群体的同步节律性放电所致，并且通过正反馈得以促进，即振荡场进一步将募集到的浦肯野细胞锁相到相同的节律性放电模式上。
