Linked Life Data

11102459

Source:http://linkedlifedata.com/resource/pubmed/id/11102459

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pubmed-article:11102459pubmed:abstractTextIt 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.lld:pubmed
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pubmed-article:11102459pubmed:articleTitleThe status of voltage-dependent calcium channels in alpha 1E knock-out mice.lld:pubmed
pubmed-article:11102459pubmed:affiliationMouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA.lld:pubmed
pubmed-article:11102459pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11102459pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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