RT Journal Article SR Electronic T1 The Status of Voltage-Dependent Calcium Channels in α1E Knock-Out Mice JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 8566 OP 8571 DO 10.1523/JNEUROSCI.20-23-08566.2000 VO 20 IS 23 A1 Wilson, Scott M. A1 Toth, Peter T. A1 Oh, Seog Bae A1 Gillard, Samantha E. A1 Volsen, Steven A1 Ren, Dongjun A1 Philipson, Louis H. A1 Lee, E. Chiang A1 Fletcher, Colin F. A1 Tessarollo, Lino A1 Copeland, Neal G. A1 Jenkins, Nancy A. A1 Miller, Richard J. YR 2000 UL http://www.jneurosci.org/content/20/23/8566.abstract 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.