Source:http://linkedlifedata.com/resource/pubmed/id/10863995
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2000-8-16
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| pubmed:abstractText |
The voltage-gated K+ channel Kv3.1 is expressed in skeletal muscle and in GABAergic interneurons in the central nervous system. Hence, the absence of Kv3.1 K+ channels may lead to a phenotype of myogenic or neurogenic origin, or both. Kv3.1-deficient (Kv3.1-/-) 129/Sv mice display altered contractile properties of their skeletal muscles and show poor performance on a rotating rod. In contrast, Kv3.1-/- mice on the (129/Sv x C57BL/6)F1 background display normal muscle properties and perform like wild-type mice. The correlation of poor performance on the rotating rod with altered muscle properties supports the notion that the skeletal muscle dysfunction in Kv3.1-/- 129/Sv mice may be responsible for the impaired motor skills on the rotating rod. Surprisingly, we did not find major differences between wild-type and Kv3.1-/- 129/Sv skeletal muscles in either the resting or action potential, the delayed-rectifier potassium conductance (gK) or the distribution of fast and slow muscle fibers. These findings suggest that the Kv3.1 K+ channel may not play a major role in the intrinsic excitability of skeletal muscle fibers although its absence leads to slower contraction and relaxation and to smaller forces in muscles of 129/Sv Kv3.1-/- mice.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Delayed Rectifier Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Myosins,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated,
http://linkedlifedata.com/resource/pubmed/chemical/Shaw Potassium Channels
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0031-6768
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
440
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
34-41
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:10863995-Action Potentials,
pubmed-meshheading:10863995-Animals,
pubmed-meshheading:10863995-Delayed Rectifier Potassium Channels,
pubmed-meshheading:10863995-Female,
pubmed-meshheading:10863995-Male,
pubmed-meshheading:10863995-Mice,
pubmed-meshheading:10863995-Mice, Inbred Strains,
pubmed-meshheading:10863995-Mice, Knockout,
pubmed-meshheading:10863995-Motor Skills Disorders,
pubmed-meshheading:10863995-Muscle, Skeletal,
pubmed-meshheading:10863995-Muscle Contraction,
pubmed-meshheading:10863995-Muscle Fibers, Skeletal,
pubmed-meshheading:10863995-Muscular Diseases,
pubmed-meshheading:10863995-Myosins,
pubmed-meshheading:10863995-Neuropeptides,
pubmed-meshheading:10863995-Potassium,
pubmed-meshheading:10863995-Potassium Channels,
pubmed-meshheading:10863995-Potassium Channels, Voltage-Gated,
pubmed-meshheading:10863995-Shaw Potassium Channels
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| pubmed:year |
2000
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| pubmed:articleTitle |
Muscle and motor-skill dysfunction in a K+ channel-deficient mouse are not due to altered muscle excitability or fiber type but depend on the genetic background.
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| pubmed:affiliation |
Department of Pharmacology, Mexico DF, Mexico.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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