PT - JOURNAL ARTICLE AU - Wilson, Scott M. AU - Toth, Peter T. AU - Oh, Seog Bae AU - Gillard, Samantha E. AU - Volsen, Steven AU - Ren, Dongjun AU - Philipson, Louis H. AU - Lee, E. Chiang AU - Fletcher, Colin F. AU - Tessarollo, Lino AU - Copeland, Neal G. AU - Jenkins, Nancy A. AU - Miller, Richard J. TI - The Status of Voltage-Dependent Calcium Channels in α<sub>1E</sub> Knock-Out Mice AID - 10.1523/JNEUROSCI.20-23-08566.2000 DP - 2000 Dec 01 TA - The Journal of Neuroscience PG - 8566--8571 VI - 20 IP - 23 4099 - http://www.jneurosci.org/content/20/23/8566.short 4100 - http://www.jneurosci.org/content/20/23/8566.full SO - J. Neurosci.2000 Dec 01; 20 AB - It has been hypothesized that R-type Ca currents result from the expression of the α1E gene. To test this hypothesis we examined the properties of voltage-dependent Ca channels in mice in which the α1E Ca channel subunit had been deleted. Application of ω-conotoxin GVIA, ω-agatoxin IVA, and nimodipine to cultured cerebellar granule neurons from wild-type mice inhibited components of the whole-cell Ba current, leaving a “residual” R current with an amplitude of ∼30% of the total Ba current. A minor portion of this R current was inhibited by the α1E-selective toxin SNX-482, indicating that it resulted from the expression of α1E. However, the majority of the R current was not inhibited by SNX-482. The SNX-482-sensitive portion of the granule cell R current was absent from α1E knock-out mice. We also identified a subpopulation of dorsal root ganglion (DRG) neurons from wild-type mice that expressed an SNX-482-sensitive component of the R current. However as with granule cells, most of the DRG R current was not blocked by SNX-482. We conclude that there exists a component of the R current that results from the expression of the α1E Ca channel subunit but that the majority of R currents must result from the expression of other Ca channel α subunits.