title: The status of voltage-dependent calcium channels in alpha 1E knock-out mice.
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.
authors: Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA.
authors: S M
authors: SM
authors: Wilson
authors: P T
authors: PT
authors: Toth
authors: S B
authors: SB
authors: Oh
authors: S E
authors: SE
authors: Gillard
authors: S
authors: S
authors: Volsen
authors: D
authors: D
authors: Ren
authors: L H
authors: LH
authors: Philipson
authors: E C
authors: EC
authors: Lee
authors: C F
authors: CF
authors: Fletcher
authors: L
authors: L
authors: Tessarollo
authors: N G
authors: NG
authors: Copeland
authors: N A
authors: NA
authors: Jenkins
authors: R J
authors: RJ
authors: Miller
mesh_terms: D000818:Animals; D001464:Barium / Q000494:pharmacology; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020908:Calcium Channels, R-Type / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism*; D002470:Cell Survival / Q000235:genetics; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D004594:Electrophysiology; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D017136:Ion Transport / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009553:Nimodipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D021122:Protein Subunits; D013111:Spider Venoms / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects; D020867:omega-Agatoxin IVA / Q000494:pharmacology; D020866:omega-Conotoxin GVIA / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020908:Calcium Channels, R-Type; D021122:Protein Subunits; C115521:SNX 482; D013111:Spider Venoms; D020867:omega-Agatoxin IVA; D001464:Barium; D009553:Nimodipine; D020866:omega-Conotoxin GVIA; D002118:Calcium