Linked Life Data

8413937

Source:http://linkedlifedata.com/resource/pubmed/id/8413937

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-11-23
pubmed:abstractText
Entry of Ca2+ through voltage-dependent Ca2+ channels is known to be linked to the exocytotic release of transmitter from sympathetic neurons. In this paper we provide evidence that transmitter release can also be stimulated by Ca2+ influx via the Na-Ca exchanger. Furthermore, the release linked to Na-Ca exchange is regulated by cardiac target cells. Cultured sympathetic neurons of the chick embryo incubated in Ca2(+)-Mg(2+)-free Krebs solution for 20 min and then switched to Ca(2+)-containing solution exhibited 15-20-fold increases in [3H]noradrenaline release over the spontaneous release. Electrophysiologic studies showed that neurons were completely depolarized in Ca(2+)-Mg(2+)-free medium. Indo-1 fluorescence revealed a large and sustained increase in intracellular free Ca2+ concentration ([Ca2+]i) after addition of Ca2+ to Ca(2+)-Mg(2+)-free medium. The increased [3H]noradrenaline release and [Ca2+]i were dependent on external Na+ and Ca2+, but were not affected by the Ca2+ channel blockers lanthanum, cadmium, verapamil or omega-conotoxin. A conventional depolarizing stimulus (125 mM K+) produced a 13-fold increase in [3H]noradrenaline release over spontaneous release. However, K(+)-induced release and rise in [Ca2+]i declined rapidly and were sensitive to the Ca2+ channel blockers. When sympathetic neurons were co-cultured with embryonic cardiac cells the release induced by change from Ca(2+)-Mg(2+)-free to Ca(2+)-Krebs solution was dramatically reduced. The change from Ca(2+)-Mg(2+)-free to Ca(2+)-Krebs solution was ineffective in evoking [3H]noradrenaline release from sympathetic neurons in situ using perfused hearts of 15-day-old chick embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
813-21
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8413937-Animals, pubmed-meshheading:8413937-Calcium, pubmed-meshheading:8413937-Calcium Channel Blockers, pubmed-meshheading:8413937-Calcium Channels, pubmed-meshheading:8413937-Carrier Proteins, pubmed-meshheading:8413937-Cell Communication, pubmed-meshheading:8413937-Cells, Cultured, pubmed-meshheading:8413937-Chick Embryo, pubmed-meshheading:8413937-Exocytosis, pubmed-meshheading:8413937-Ganglia, Sympathetic, pubmed-meshheading:8413937-Magnesium, pubmed-meshheading:8413937-Membrane Potentials, pubmed-meshheading:8413937-Myocardium, pubmed-meshheading:8413937-Nerve Tissue Proteins, pubmed-meshheading:8413937-Neurons, pubmed-meshheading:8413937-Norepinephrine, pubmed-meshheading:8413937-Sodium, pubmed-meshheading:8413937-Sodium-Calcium Exchanger, pubmed-meshheading:8413937-Stimulation, Chemical
pubmed:year
1993
pubmed:articleTitle
Massive exocytosis triggered by sodium-calcium exchange in sympathetic neurons is attenuated by co-culture with cardiac cells.
pubmed:affiliation
Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't