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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1997-11-6
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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.
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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/Buffers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Central Nervous System Depressants,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Ethanol,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
8
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pubmed:volume |
765
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
30-6
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9310391-Action Potentials,
pubmed-meshheading:9310391-Animals,
pubmed-meshheading:9310391-Buffers,
pubmed-meshheading:9310391-Calcium Channels,
pubmed-meshheading:9310391-Central Nervous System Depressants,
pubmed-meshheading:9310391-Electrophysiology,
pubmed-meshheading:9310391-Enzyme Activation,
pubmed-meshheading:9310391-Enzyme Inhibitors,
pubmed-meshheading:9310391-Ethanol,
pubmed-meshheading:9310391-GTP-Binding Proteins,
pubmed-meshheading:9310391-Ganglia, Invertebrate,
pubmed-meshheading:9310391-Helix (Snails),
pubmed-meshheading:9310391-Neurons,
pubmed-meshheading:9310391-Protein Kinase Inhibitors,
pubmed-meshheading:9310391-Protein Kinases,
pubmed-meshheading:9310391-Signal Transduction
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pubmed:year |
1997
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pubmed:articleTitle |
Ethanol suppresses neuronal Ca2+ currents by effects on intracellular signal transduction.
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pubmed:affiliation |
Department of Physiology, Institute of Zoology, University of Salzburg, Austria.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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