期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1989
卷号：86
期号：18
页码：7228-7232
DOI：10.1073/pnas.86.18.7228
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Thalamic neurons undergo a shift from tonic to phasic (burst) firing upon hyperpolarization. This state transition results from deinactivation of a regenerative depolarizing event referred to as the low-threshold spike. Isolated adult guinea pig thalamic (dorsal lateral geniculate) neurons exhibited low-threshold spikes that could be blocked by low concentrations of nickel but were unaffected by the dihydropyridine nimodipine. Whole-cell voltage-clamp recordings from these cells demonstrated a low-threshold, rapidly inactivating (T) Ca2+ current that manifested similar voltage dependency and time course as the low-threshold spike. Like low-threshold spikes, the T-type Ca2+ current was eliminated by nickel but was unaffected by nimodipine. In thalamic neurons, T-type Ca2+ channels underlie the low-threshold spike and, therefore, play a critical role in regulating the firing pattern of these cells.
