Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-11-6
pubmed:abstractText
The mechanism of action of ethanol on voltage-activated Ca2+ currents in neurons of the mollusk, Helix pomatia, was studied focusing on intracellular signaling. Ethanol suppressed inward Ca2+ currents in a time- and voltage-dependent manner. Buffering of intracellular Ca2+ with bis(o-aminophenoxy)ethane-N,N,N',N-tetraacetic acid (BAPTA) abolished the ethanol effects on Ca2+ currents. Intracellular GTP-gamma-S injection decreased Ca2+ currents whereas GDP-beta-S injection was ineffective. Ethanol had no further blocking effect on Ca2+ currents in GTP-gamma-S injected cells. In the presence of dopamine, which is known to suppress Ca2+ currents by G0-protein activation, ethanol application was ineffective. The protein kinase C (PKC) blockers, staurosporine and chelerythrine, prevented the ethanol effects on Ca2+ currents. The PKC activators, 1,2-oleoylacetylglycerol (OAG) and beta-phorbol-12,13-dibutyrate (PdBu), both, after maximum stimulation, also occluded the effect of ethanol on Ca2+ currents, whereas in the presence of 4-alpha-phorbol-12,13-didecanoate (4-alpha-PDD), an ineffective phorbol ester, ethanol suppressed Ca2+ currents. Ethanol increased the threshold of Ca2+-dependent action potentials and decreased their duration. Our results indicate that the suppression of voltage-activated Ca2+ currents by ethanol and its effects on action potentials involve activation of a G-protein/protein kinase transduction pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
765
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
30-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Ethanol suppresses neuronal Ca2+ currents by effects on intracellular signal transduction.
pubmed:affiliation
Department of Physiology, Institute of Zoology, University of Salzburg, Austria.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't