The status of voltage-dependent calcium channels in α(1E) knock-out mice

S. M. Wilson, P. T. Toth, S. B. Oh, S. E. Gillard, S. Volsen, D. Ren, L. H. Philipson, E. Chiang Lee, C. F. Fletcher, L. Tessarollo, N. G. Copeland, N. A. Jenkins, R. J. Miller

Research output: Contribution to journalArticle

123 Scopus citations

Abstract

It has been hypothesized that R-type Ca currents result from the expression of the α1(E) gene. To test this hypothesis we examined the properties of voltage-dependent Ca channels in mice in which the α1(E) Ca channel subunit had been deleted. Application of θ-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 α1(E)-selective toxin SNX-482, indicating that it resulted from the expression of α1(E). 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 α1(E) 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 α1(E) Ca channel subunit but that the majority of R currents must result from the expression of other Ca channel α subunits.

Original languageEnglish (US)
Pages (from-to)8566-8571
Number of pages6
JournalJournal of Neuroscience
Volume20
Issue number23
DOIs
StatePublished - Dec 1 2000

Keywords

  • α(E) knock-out mice
  • Cerebellar granule cells
  • Dorsal root ganglia
  • Pain
  • Synaptic transmission
  • Voltage-dependent calcium channels

ASJC Scopus subject areas

  • Neuroscience(all)

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