Source:http://linkedlifedata.com/resource/pubmed/id/10323308
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rdf:type | |
lifeskim:mentions |
umls-concept:C0027882,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0086376,
umls-concept:C0439799,
umls-concept:C0521116,
umls-concept:C0596235,
umls-concept:C0597357,
umls-concept:C0729936,
umls-concept:C1522207,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1879547,
umls-concept:C1948027
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pubmed:issue |
1
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pubmed:dateCreated |
1999-6-17
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pubmed:abstractText |
In the present study, we examined the ability of several putative neurotransmitters and neuromodulators to modulate voltage-dependent Ca2+ channel currents in adult rat intracardiac neurons. Of 17 compounds tested, acetylcholine (Ach), neuropeptide Y (NPY), norepinephrine (NE), and met-enkephalin (met-Enk) were effective modulators of the Ca2+ currents. The neurotransmitter-induced current inhibition was associated with slow activation kinetics and relief by a strong depolarizing prepulse. Overnight pretreatment of neurons with pertussis toxin (PTX, 500 ng/ml) significantly attenuated the neurotransmitter-induced current inhibition. Heterologous expression of transducin, a known chelator of G-protein betagamma subunits, almost completely abolished the neurotransmitter-induced current inhibition. Taken together, our data suggest that four different neurotransmitters inhibit the Ca2+ channel currents in adult rat intracardiac neurons via a pathway that is voltage-dependent, membrane-delimited, and utilizes betagamma subunits released from PTX-sensitive G-proteins. The Ca2+ channel inhibition by non-cholinergic neurotransmitters may play important roles in regulation of neuronal excitability and Ach release at synapses in intracardiac ganglia, thereby contributing to cholinergic control of cardiac functions.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Transducin,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0165-1838
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
68-74
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10323308-Animals,
pubmed-meshheading:10323308-Calcium Channels,
pubmed-meshheading:10323308-Electric Conductivity,
pubmed-meshheading:10323308-Electrophysiology,
pubmed-meshheading:10323308-GTP-Binding Proteins,
pubmed-meshheading:10323308-Heart Conduction System,
pubmed-meshheading:10323308-Male,
pubmed-meshheading:10323308-Neurons,
pubmed-meshheading:10323308-Neurotransmitter Agents,
pubmed-meshheading:10323308-Pertussis Toxin,
pubmed-meshheading:10323308-Rats,
pubmed-meshheading:10323308-Rats, Sprague-Dawley,
pubmed-meshheading:10323308-Receptors, Cell Surface,
pubmed-meshheading:10323308-Transducin,
pubmed-meshheading:10323308-Virulence Factors, Bordetella
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pubmed:year |
1999
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pubmed:articleTitle |
Activation of various G-protein coupled receptors modulates Ca2+ channel currents via PTX-sensitive and voltage-dependent pathways in rat intracardiac neurons.
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pubmed:affiliation |
Laboratory of Molecular Physiology, Guthrie Research Institute, Sayre, PA 18840, USA. sjeong@inet.guthrie.org
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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