Source:http://linkedlifedata.com/resource/pubmed/id/20054822
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-2-1
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pubmed:abstractText |
Patch-clamp experiments were performed to investigate the behavior of voltage-activated inward currents in vas deferens myocytes from Na(V)1.6-null mice (Na(V)1.6(-/-)) lacking the expression of the Na(+) channel gene, Scn8a, and their wild-type littermates (Na(V)1.6(+/+)). Immunohistochemistry confirmed expression of Na(V)1.6 in the muscle of Na(V)1.6(+/+), but not Na(V)1.6(-/-), vas deferens. PCR analysis revealed that the only beta(1)-subunit gene expressed in Na(V)1.6(+/+) vas deferens was Scn1b. In Na(V)1.6(+/+) myocytes, the threshold for membrane currents evoked by 20 msec voltage ramps (-100 mV to 60 mV) was -38.5 +/- 4.6 mV and this was shifted to a more positive potential (-31.2 +/- 4.9 mV) by tetrodotoxin (TTX). In Na(V)1.6(-/-) myocytes, the threshold was -30.4 +/- 3.4 mV and there was no TTX-sensitive current. The Na(+) current (I(Na)) in Na(V)1.6(+/+) myocytes had a bell-shaped current-voltage relationship that peaked at approximately -10 mV. Increasing the duration of the voltage ramps beyond 20 msec reduced the peak amplitude of I(Na). I(Na) displayed both fast (tau approximately 10 msec) and slow (tau approximately 1 sec) recovery from inactivation, the magnitude of the slow component increasing with the duration of the conditioning pulse (5-40 msec). During repetitive activation (5-40 msec pulses), I(Na) declined at stimulation frequencies > 0.5 Hz and at 10 Hz <or= 50% of the current remained. These findings indicate that I(Na) is due solely to Na(V)1.6 in Na(V)1.6(+/+) myocytes. The gating properties of these channels suggest they play a major role in regulating smooth muscle excitability, particularly in response to rapid depolarizing stimuli.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Scn1b protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Scn8a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1097-4652
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pubmed:author | |
pubmed:copyrightInfo |
J. Cell. Physiol. 223: 234-243, 2010. (c) 2010 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
223
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
234-43
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pubmed:meshHeading |
pubmed-meshheading:20054822-Animals,
pubmed-meshheading:20054822-Cell Separation,
pubmed-meshheading:20054822-Electric Stimulation,
pubmed-meshheading:20054822-Immunohistochemistry,
pubmed-meshheading:20054822-Ion Channel Gating,
pubmed-meshheading:20054822-Kinetics,
pubmed-meshheading:20054822-Male,
pubmed-meshheading:20054822-Membrane Potentials,
pubmed-meshheading:20054822-Mice,
pubmed-meshheading:20054822-Mice, Inbred C3H,
pubmed-meshheading:20054822-Mice, Knockout,
pubmed-meshheading:20054822-Muscle, Smooth,
pubmed-meshheading:20054822-Myocytes, Smooth Muscle,
pubmed-meshheading:20054822-Nerve Tissue Proteins,
pubmed-meshheading:20054822-Patch-Clamp Techniques,
pubmed-meshheading:20054822-RNA, Messenger,
pubmed-meshheading:20054822-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20054822-Sodium,
pubmed-meshheading:20054822-Sodium Channel Blockers,
pubmed-meshheading:20054822-Sodium Channels,
pubmed-meshheading:20054822-Tetrodotoxin,
pubmed-meshheading:20054822-Vas Deferens
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pubmed:year |
2010
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pubmed:articleTitle |
Characterization of NaV1.6-mediated Na+ currents in smooth muscle cells isolated from mouse vas deferens.
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pubmed:affiliation |
Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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