Linked Life Data

9362250

Source:http://linkedlifedata.com/resource/pubmed/id/9362250

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 2
pubmed:dateCreated
1997-12-10
pubmed:abstractText
The aim of this study was to investigate modulation of voltage-dependent steady-state activation and availability from inactivation of the cardiac Na+ channel by the cytoskeleton. As an experimental approach, we used long-lasting monitoring [63 +/- 5 (SE) min] of the half-point potentials of the steady-state availability curve (V(1/2A)) and normalized conductance curve (V(1/2G)) in 116 rat ventricular cardiomyocytes by whole cell patch clamp at 22-24 degrees C. Both half-point potentials shifted in the negative direction with time as an exponentially saturating change, with the shift of V(1/2G) being smaller and faster. An F-actin disrupter, cytochalasin D (Cyto-D, 20 microM), accelerated the rate of the V(1/2A) shift but decreased the range of the V(1/2G) shift. An F-actin stabilizer, phalloidin (100 microM), temporarily (for 28.2 +/- 2.2 min, n = 15) prevented the V(1/2A) shift but did not influence the V(1/2G) shift. The best fit for the V(1/2G)-V(1/2A) relationship in untreated cells (1,021 data points measured in 51 cells) was a second-degree (2.06) power function. Cytoskeleton-directed agents modified the relationship. In Cyto-D-treated cells, the V(1/2G)-V(1/2A) relationship was shifted (by 2.5 mV) toward positive V(1/2G). On the contrary, a microtubule stabilizer, taxol (100 microM), shifted the relationship toward negative V(1/2G) (by 12.2 mV). We conclude that coupling between availability and activation is modulated by F-actin-based and microtubular cytoskeleton.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
273
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1832-40
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Cytoskeleton modulates coupling between availability and activation of cardiac sodium channel.
pubmed:affiliation
Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan 48202-2689, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.