rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1310
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pubmed:dateCreated |
1991-10-8
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pubmed:abstractText |
The predominant consequences of mu-opioid-receptor activation are depression of both neuronal activity and transmitter release. Mu-Opioid agonists have previously been observed to increase a potassium conductance and to inhibit adenylate cyclase. We now report that activation of mu-opioid receptors directly decreases the N-type calcium-channel current in a differentiated, human neuroblastoma cell line (SH-SY5Y). The coupling between the mu-opioid receptor and the calcium channel involves a pertussis toxin-sensitive G protein and is independent of changes in adenylate cyclase activity. The inhibition of the calcium-channel current is voltage dependent because it is largely overcome by strong membrane depolarization. It is not associated with changes in the kinetics of current inactivation. Therefore, the mu-receptor belongs to the superfamily of G-protein-coupled, inhibitory neurotransmitter receptors which modulate the activity of calcium and potassium channels and adenylate cyclase.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, Ala(2)-MePhe(4)-Gly(5)-,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalins,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Naloxone,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0962-8452
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
244
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
129-35
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1679547-Adenylate Cyclase,
pubmed-meshheading:1679547-Adenylate Cyclase Toxin,
pubmed-meshheading:1679547-Calcium Channels,
pubmed-meshheading:1679547-Enkephalin, Ala(2)-MePhe(4)-Gly(5)-,
pubmed-meshheading:1679547-Enkephalins,
pubmed-meshheading:1679547-GTP-Binding Proteins,
pubmed-meshheading:1679547-Humans,
pubmed-meshheading:1679547-Membrane Potentials,
pubmed-meshheading:1679547-Naloxone,
pubmed-meshheading:1679547-Pertussis Toxin,
pubmed-meshheading:1679547-Receptors, Opioid,
pubmed-meshheading:1679547-Receptors, Opioid, mu,
pubmed-meshheading:1679547-Tumor Cells, Cultured,
pubmed-meshheading:1679547-Virulence Factors, Bordetella
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pubmed:year |
1991
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pubmed:articleTitle |
Mu-opioid-receptor-mediated inhibition of the N-type calcium-channel current.
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pubmed:affiliation |
Department of Pharmacology, University of Cambridge, U.K.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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