Publications [#381484] of Seog Oh

Papers Published

1. Wilson, SM; Toth, PT; Oh, SB; Gillard, SE; Volsen, S; Ren, D; Philipson, LH; Lee, EC; Fletcher, CF; Tessarollo, L; Copeland, NG; Jenkins, NA; Miller, RJ, The status of voltage-dependent calcium channels in alpha 1E knock-out mice., The Journal of neuroscience : the official journal of the Society for Neuroscience, vol. 20 no. 23 (December, 2000), pp. 8566-8571 [doi]
   (last updated on 2026/01/20)

   Abstract:
   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.