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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006675,
umls-concept:C0006685,
umls-concept:C0013782,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0027747,
umls-concept:C0030685,
umls-concept:C0231491,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C0752346,
umls-concept:C1167622,
umls-concept:C1283071,
umls-concept:C1707723,
umls-concept:C1963578
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pubmed:issue |
1-2
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pubmed:dateCreated |
1988-9-15
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pubmed:abstractText |
We have previously shown that the calcium channel antagonist omega-conotoxin M-VII-A blocks neurotransmitter release from isolated nerve terminals (synaptosomes) from the electric organ of the electric ray (Yeager et al., J. Neurosci., 7 (1987) 2390-2396). We now demonstrate that a related but more readily available peptide, omega-conotoxin G-VI-A (CgTx), also blocks the release of transmitter from these terminals and, in addition, inhibits depolarization-dependent uptake of Ca2+ into these terminals. The half-maximal inhibitory concentration (IC50 for block of depolarization-evoked release and for depolarization-dependent uptake of Ca2+ are approximately 3 and 2 microM, respectively. These results suggest the inhibitory effects of CgTx are due to the inhibition of Ca2+ entry into synaptosomes through voltage-sensitive calcium channels. Assays of radioiodinated CgTx binding to electric organ synaptosomal membranes and synaptosomes appear to show a single binding site with an apparent dissociation constant (Kd) of 3-5 microM and toxin receptor densities of 290 and 52 pmol/mg protein, respectively. These CgTx receptor densities are equivalent to 6% of the total synaptosomal membrane protein and 1% of the total synaptosomal protein (assuming a molecular weight of 200 kDa for the toxin receptor). If the observed CgTx receptor densities reflect the actual densities of voltage-sensitive calcium channels in electric organ synaptosomal membranes and synaptosomes, these preparations would be the richest source of these channels yet described.
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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/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Cadmium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Mollusk Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Conotoxin GVIA
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
453
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
247-56
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:3401762-Adenosine Triphosphate,
pubmed-meshheading:3401762-Animals,
pubmed-meshheading:3401762-Cadmium,
pubmed-meshheading:3401762-Calcium,
pubmed-meshheading:3401762-Calcium Channel Blockers,
pubmed-meshheading:3401762-Electric Fish,
pubmed-meshheading:3401762-Electric Organ,
pubmed-meshheading:3401762-Kinetics,
pubmed-meshheading:3401762-Mollusk Venoms,
pubmed-meshheading:3401762-Synaptosomes,
pubmed-meshheading:3401762-omega-Conotoxin GVIA
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pubmed:year |
1988
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pubmed:articleTitle |
The calcium channel antagonist, omega-conotoxin, and electric organ nerve terminals: binding and inhibition of transmitter release and calcium influx.
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pubmed:affiliation |
Department of Biological Sciences, University of Southern California, Los Angeles 90089-0371.
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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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