RT Journal Article
SR Electronic
T1 The Status of Voltage-Dependent Calcium Channels in α<sub>1E</sub> 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.