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：2002
卷号：99
期号：5
页码：3276-3281
DOI：10.1073/pnas.052697799
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：R-type Ca2+ channels play a critical role in coupling excitability to dendritic Ca2+ influx and neuronal secretion. Unlike other types of voltage-sensitive Ca2+ channels (L, N, P/Q, and T type), the molecular basis for the R-type Ca2+ channel is still unclear, thereby limiting further detailed analyses of R-type Ca2+ channel physiology. The prevailing hypothesis is that 1E (CaV2.3) gene encodes for R-type Ca2+ channels, but the dearth of critical evidence has rendered this hypothesis controversial. Here we generated 1E-deficient mice (1E-/-) and examined the status of voltage-sensitive Ca2+ currents in central amygdala (CeA) neurons that exhibit abundant 1E expression and R-type Ca2+ currents. The majority of R-type currents in CeA neurons were eliminated in 1E-/- mice whereas other Ca2+ channel types were unaffected. These data clearly indicate that the expression of 1E gene underlies R-type Ca2+ channels in CeA neurons. Furthermore, the 1E-/- mice exhibited signs of enhanced fear as evidenced by their vigorous escaping behavior and aversion to open-field conditions. These latter findings imply a possible role of 1E-based R-type Ca2+ currents in amygdala physiology associated with fear.
