Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-2-1
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1097-4652
pubmed:author
pubmed:copyrightInfo
J. Cell. Physiol. 223: 234-243, 2010. (c) 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
223
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
234-43
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
pubmed:year
2010
pubmed:articleTitle
Characterization of NaV1.6-mediated Na+ currents in smooth muscle cells isolated from mouse vas deferens.
pubmed:affiliation
Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't