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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1991-11-25
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pubmed:abstractText |
Effects of acetylcholine (ACh) and noradrenaline (NA) on voltage-gated ion channels of sympathetic neurones acutely dissociated from rat superior cervical ganglion (SCG) were examined using the whole-cell voltage-clamp technique. Depolarizing voltage steps elicited two types of low- and high-voltage-activated (LVA and HVA) Ca2+ currents. Pressure applications of ACh and NA produced concentration-dependent inhibition of the HVA Ca2+ current without affecting the LVA Ca2+ current. The inhibitory action of ACh on the Ca2+ current was blocked by a muscarinic antagonist, atropine. The action of NA was suppressed by an alpha 2-adrenergic antagonist, yohimbine, but not by an alpha 1-adrenergic antagonist, prazosin. Delayed rectifying outward K+ currents and inward rectifying K+ current were not affected by either ACh or NA. Tetrodotoxin-sensitive and -insensitive Na+ currents also remained unaffected under actions of ACh and NA. When recorded with electrode containing guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S), the inhibitory actions of ACh and NA on Ca2+ currents became irreversible. After treatment of SCG neurones with pertussis toxin, the inhibitory action of ACh on the Ca2+ current was almost completely abolished, whereas the action of NA was only partially reduced. The results suggest that ACh and NA differentially inhibit the HVA Ca2+ current via different G proteins coupling muscarinic and alpha 2-adrenergic receptors to Ca2+ channels in rat SCG neurones.
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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/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Muscarinic,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
418
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
592-600
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:1658727-Acetylcholine,
pubmed-meshheading:1658727-Adenylate Cyclase,
pubmed-meshheading:1658727-Animals,
pubmed-meshheading:1658727-Calcium Channels,
pubmed-meshheading:1658727-GTP-Binding Proteins,
pubmed-meshheading:1658727-Ganglia, Sympathetic,
pubmed-meshheading:1658727-Neurons,
pubmed-meshheading:1658727-Norepinephrine,
pubmed-meshheading:1658727-Pertussis Toxin,
pubmed-meshheading:1658727-Potassium,
pubmed-meshheading:1658727-Protein Kinase C,
pubmed-meshheading:1658727-Rats,
pubmed-meshheading:1658727-Receptors, Adrenergic,
pubmed-meshheading:1658727-Receptors, Muscarinic,
pubmed-meshheading:1658727-Virulence Factors, Bordetella
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pubmed:year |
1991
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pubmed:articleTitle |
Adrenergic and cholinergic inhibition of Ca2+ channels mediated by different GTP-binding proteins in rat sympathetic neurones.
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pubmed:affiliation |
Laboratory of Cellular Physiology, Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro
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