| First Author | Wilson SM | Year | 2000 |
| Journal | J Neurosci | Volume | 20 |
| Issue | 23 | Pages | 8566-71 |
| PubMed ID | 11102459 | Mgi Jnum | J:66144 |
| Mgi Id | MGI:1928028 | Doi | 10.1523/JNEUROSCI.20-23-08566.2000 |
| Citation | Wilson SM, et al. (2000) The status of voltage-dependent calcium channels in alpha 1E knock-Out mice. J Neurosci 20(23):8566-71 |
| abstractText | It has been hypothesized that R-type Ca currents result from the expression of the alpha(1E) gene. To test this hypothesis we examined the properties of voltage-dependent Ca channels in mice in which the alpha(1E) Ca channel subunit had been deleted. Application of omega-conotoxin GVIA, omega-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 approximately 30% of the total Ba current. A minor portion of this R current was inhibited by the alpha(1E)-selective toxin SNX-482, indicating that it resulted from the expression of alpha(1E). 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 alpha(1E) 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 alpha(1E) Ca channel subunit but that the majority of R currents must result from the expression of other Ca channel alpha subunits. |
