Shin Hee-Sup
Center for Neural Science, Korea Institute of Science and Technology, 39-1 Hawolgok-dong, Seongbuk-ku, Seoul 136-791, Republic of Korea.
Cell Calcium. 2006 Aug;40(2):191-6. doi: 10.1016/j.ceca.2006.04.023. Epub 2006 Jun 13.
Burst firing of the thalamic neurons is driven by the low threshold Ca2+ spike generated by Ca2+ influx through T-type Ca2+ channels when these channels are activated by membrane hyperpolarization due to inhibitory inputs. The major inhibitory inputs to the thalamocortical (TC) neurons are from the GABAergic neurons in the thalamic reticular nucleus. Thalamic burst firings have long been implicated in the pathogenesis of absence epilepsy. The recent progress in genetic approaches has provided with an opportunity to examine this issue at the level of an organism. In this review I describe results primarily obtained from the analysis of the mice deficient for the alpha1G locus which is the predominant gene underlying the low threshold Ca2+ currents in the TC neurons. Current results so far demonstrate the essential role of the thalamocortical bursts in certain forms of absence seizures. Understanding of the pathophysiological mechanisms of absence epilepsy may help develop drugs to control the disease.
丘脑神经元的爆发式放电是由低阈值Ca2+尖峰驱动的，当这些通道因抑制性输入导致膜超极化而被激活时，Ca2+通过T型Ca2+通道内流产生低阈值Ca2+尖峰。丘脑皮质（TC）神经元的主要抑制性输入来自丘脑网状核中的GABA能神经元。丘脑爆发式放电长期以来一直被认为与失神癫痫的发病机制有关。遗传方法的最新进展为在生物体水平上研究这个问题提供了机会。在这篇综述中，我描述了主要通过对缺乏α1G基因座的小鼠进行分析而获得的结果，α1G基因座是TC神经元中低阈值Ca2+电流的主要基础基因。目前的结果表明，丘脑皮质爆发在某些形式的失神发作中起着至关重要的作用。了解失神癫痫的病理生理机制可能有助于开发控制该疾病的药物。
