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.