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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1996-12-4
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pubmed:abstractText |
1. Whole-cell patch-clamp recording were employed to study facilitation of Ca2+ currents and excessive Ca2+ tail currents evoked by strong and long-lasting conditioning depolarizations in skeletal myoballs cultured from newborn rats. 2. Paired-pulse facilitation and excessive tail currents showed the same voltage dependence, becoming prominent at conditioning potentials above +30 mV. 3. Recruitment of excessive tail currents and facilitation occurred with the same time dependence (time constant (tau), approximately 200 ms to approximately 1 s), accelerating with the depolarization strength of conditioning pulses. 4. Reversal of Ca2+ current facilitation during the repolarization period between conditioning and test pulses was time- and voltage dependent. The time window of recruitment of facilitated Ca2+ currents narrowed considerably at more negative repolarization potentials (tau: approximately 10 ms at -100 mV, but approximately 1.5 at 0 mV). 5. Neither omission of internal ATP nor perfusion of the cells with the peptide inhibitor of protein kinase A (PKI) had significant effects on Ca2+ current facilitation, although internal perfusion with ATP gamma S slowly suppressed the facilitation currents by about 30%. External application of either ryanodine or caffeine under control conditions selectively and significantly suppressed the facilitated Ca2+ currents by about 30-40%. 6. We propose that facilitation of Ca2+ currents and excessive tail currents are consequences of a common mechanism linked to ryanodine receptors.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-1319555,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-1654413,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-1715918,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-1970471,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2155470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2155471,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2158764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2164405,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2166917,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2170630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2447504,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-2567963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-6091117,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-6296372,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-7693682,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-7972090,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-8245124,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-8391648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8814612-8583414
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-3751
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
494 ( Pt 1)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
141-53
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading | |
pubmed:year |
1996
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pubmed:articleTitle |
Silent calcium channels generate excessive tail currents and facilitation of calcium currents in rat skeletal myoballs.
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pubmed:affiliation |
Department of Membrane Biophysics, 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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