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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
23
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pubmed:dateCreated |
2001-1-4
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pubmed: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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, R-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Nimodipine,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/SNX 482,
http://linkedlifedata.com/resource/pubmed/chemical/Spider Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Agatoxin IVA,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Conotoxin GVIA
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1529-2401
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pubmed:author |
pubmed-author:CopelandN GNG,
pubmed-author:FletcherC FCF,
pubmed-author:GillardS ESE,
pubmed-author:JenkinsN ANA,
pubmed-author:LeeE CEC,
pubmed-author:MillerR JRJ,
pubmed-author:OhS BSB,
pubmed-author:PhilipsonL HLH,
pubmed-author:ReeMM,
pubmed-author:TessarolloLL,
pubmed-author:TothP TPT,
pubmed-author:VolsenSS,
pubmed-author:WilsonS MSM
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
8566-71
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11102459-Animals,
pubmed-meshheading:11102459-Barium,
pubmed-meshheading:11102459-Blotting, Western,
pubmed-meshheading:11102459-Calcium,
pubmed-meshheading:11102459-Calcium Channel Blockers,
pubmed-meshheading:11102459-Calcium Channels, R-Type,
pubmed-meshheading:11102459-Cell Survival,
pubmed-meshheading:11102459-Cells, Cultured,
pubmed-meshheading:11102459-Cerebellum,
pubmed-meshheading:11102459-Electrophysiology,
pubmed-meshheading:11102459-Ganglia, Spinal,
pubmed-meshheading:11102459-Ion Transport,
pubmed-meshheading:11102459-Mice,
pubmed-meshheading:11102459-Mice, Inbred C57BL,
pubmed-meshheading:11102459-Mice, Knockout,
pubmed-meshheading:11102459-Neurons,
pubmed-meshheading:11102459-Nimodipine,
pubmed-meshheading:11102459-Patch-Clamp Techniques,
pubmed-meshheading:11102459-Protein Subunits,
pubmed-meshheading:11102459-Spider Venoms,
pubmed-meshheading:11102459-Synaptic Transmission,
pubmed-meshheading:11102459-omega-Agatoxin IVA,
pubmed-meshheading:11102459-omega-Conotoxin GVIA
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pubmed:year |
2000
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pubmed:articleTitle |
The status of voltage-dependent calcium channels in alpha 1E knock-out mice.
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pubmed:affiliation |
Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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