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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1997-2-19
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pubmed:abstractText |
1. Whole-cell patch-clamp recordings were used to study voltage-dependent facilitation of Ca2+ currents and excessive Ca2+ tail current in skeletal myoballs cultured from wild-type and transgenic mice expressing a null mutation of the ryanodine receptor (RyR) type 1 (dyspedic myoballs). 2. Ca2+ current density in dyspedic myoballs was reduced by about 60% compared with wild-type cells, with dihydropyridine-binding capacity largely retained. 3. Strong and long-lasting depolarizations (+80 mV and 600 ms), which normally produce excessive tail currents upon repolarization in control cells, failed to do so in dyspedic myoballs. 4. Dyspedic myoballs also failed to produce both Ca2+ current facilitation and the left shift of the current-voltage (I-V) curve induced by paired-pulse stimulation. 5. We propose that excessive tail currents and facilitation arise from silent Ca2+ channels acting as the voltage sensors in excitation-contraction coupling.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-1328292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-2419767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-2434854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-2581141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-4540479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-6147356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-7505915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-7515481,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-7724570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-7742348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-8391648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-8405367,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-8583414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-8598910,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8910220-8814612
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
496 ( Pt 2)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
339-45
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8910220-Animals,
pubmed-meshheading:8910220-Animals, Newborn,
pubmed-meshheading:8910220-Calcium Channels,
pubmed-meshheading:8910220-Calmodulin-Binding Proteins,
pubmed-meshheading:8910220-Electrophysiology,
pubmed-meshheading:8910220-Membrane Potentials,
pubmed-meshheading:8910220-Mice,
pubmed-meshheading:8910220-Mice, Inbred C57BL,
pubmed-meshheading:8910220-Mice, Transgenic,
pubmed-meshheading:8910220-Muscle, Skeletal,
pubmed-meshheading:8910220-Muscle Proteins,
pubmed-meshheading:8910220-Mutation,
pubmed-meshheading:8910220-Patch-Clamp Techniques,
pubmed-meshheading:8910220-Ryanodine Receptor Calcium Release Channel
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pubmed:year |
1996
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pubmed:articleTitle |
Absence of Ca2+ current facilitation in skeletal muscle of transgenic mice lacking the type 1 ryanodine receptor.
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pubmed:affiliation |
Max Planck Institute for Biophysical Chemistry, Göttingen, Germany. afleig@gwdg.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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