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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
13
|
| pubmed:dateCreated |
1993-6-4
|
| pubmed:abstractText |
Evidence for activation of pertussis-toxin-sensitive G-proteins by membrane depolarization in rat brainstem synaptoneurosomes was recently reported (Cohen-Armon, M., and Sokolovsky, M. (1991) J. Biol. Chem. 266, 2595-2605; (1991) Neurosci. Lett. 126, 87-90) and is further supported in this study by the observation that the depolarization-induced effect is inhibited when G-proteins are stabilized in the non-activated state with guanosine 5'-O-(2-thiodiphosphate) (GDP beta S), which was introduced into synaptoneurosomes during the process of permeabilization and resealing. In the present study, agents that either keep the voltage-dependent Na+ channel in persistently activated state (while Na+ currents are blocked) or prevent it from activation were used in an attempt to determine whether the voltage-dependent Na+ channels are involved in the depolarization-induced activation of pertussis-toxin-sensitive G-proteins. The main probe employed was the cardiotonic and antiarrhythmic agent DPI, which is a racemic mixture of two enantiomers, one of which (the R enantiomer) reportedly prevents depolarization-induced activation of the Na+ channel while the other (the S enantiomer) inhibits Na+ channel inactivation. The results suggest that while inactivation of the voltage-dependent Na+ channel does not interfere with the putative depolarization-induced activation of G-proteins, membrane depolarization affects G-proteins and the coupled muscarinic receptors only if the voltage-dependent Na+ channels are capable of being activated. Thus, inhibition of the depolarization-induced activation of Na+ channels was accompanied by inhibition of the depolarization-induced activation of pertussis-toxin-sensitive G-proteins and by modifications of both the coupling of G-proteins to muscarinic receptors and the ADP-ribosylation of Go-proteins. These effects could be counteracted by persistent activation of the voltage-dependent Na+ channels (while Na+ current was blocked). Our observations may suggest that the voltage-dependent Na+ channel gating is involved in the depolarization-induced activation of pertussis toxin-sensitive G-proteins and may provide evidence for a possible mechanism of membrane depolarization signal transduction in excitable cells.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Diphosphate Ribose,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Arrhythmia Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Bungarotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/DPI 201-106,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine Diphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylyl Imidodiphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Muscarinic,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin,
http://linkedlifedata.com/resource/pubmed/chemical/Thionucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella,
http://linkedlifedata.com/resource/pubmed/chemical/guanosine 5'-O-(2-thiodiphosphate)
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0021-9258
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
5
|
| pubmed:volume |
268
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
9824-38
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8387506-Acetylcholine,
pubmed-meshheading:8387506-Adenosine Diphosphate Ribose,
pubmed-meshheading:8387506-Animals,
pubmed-meshheading:8387506-Anti-Arrhythmia Agents,
pubmed-meshheading:8387506-Brain Stem,
pubmed-meshheading:8387506-Bungarotoxins,
pubmed-meshheading:8387506-GTP-Binding Proteins,
pubmed-meshheading:8387506-Guanosine Diphosphate,
pubmed-meshheading:8387506-Guanosine Triphosphate,
pubmed-meshheading:8387506-Guanylyl Imidodiphosphate,
pubmed-meshheading:8387506-Ion Channel Gating,
pubmed-meshheading:8387506-Kinetics,
pubmed-meshheading:8387506-Male,
pubmed-meshheading:8387506-Membrane Potentials,
pubmed-meshheading:8387506-Molecular Weight,
pubmed-meshheading:8387506-Neurons,
pubmed-meshheading:8387506-Pertussis Toxin,
pubmed-meshheading:8387506-Piperazines,
pubmed-meshheading:8387506-Rats,
pubmed-meshheading:8387506-Rats, Inbred Strains,
pubmed-meshheading:8387506-Receptors, Muscarinic,
pubmed-meshheading:8387506-Sodium Channels,
pubmed-meshheading:8387506-Stereoisomerism,
pubmed-meshheading:8387506-Synaptosomes,
pubmed-meshheading:8387506-Tetrodotoxin,
pubmed-meshheading:8387506-Thionucleotides,
pubmed-meshheading:8387506-Virulence Factors, Bordetella
|
| pubmed:year |
1993
|
| pubmed:articleTitle |
Evidence for involvement of the voltage-dependent Na+ channel gating in depolarization-induced activation of G-proteins.
|
| pubmed:affiliation |
Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Israel.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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