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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004749,
umls-concept:C0030685,
umls-concept:C0039067,
umls-concept:C0220839,
umls-concept:C0391871,
umls-concept:C0439799,
umls-concept:C0596235,
umls-concept:C0597484,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1314939,
umls-concept:C1816453,
umls-concept:C1882598,
umls-concept:C1963578
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pubmed:issue |
4
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pubmed:dateCreated |
1993-10-21
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pubmed:abstractText |
During K(+)-induced depolarization of isolated rat brain nerve terminals (synaptosomes), 1 mM Ba2+ could substitute for 1 mM Ca2+ in evoking the release of endogenous glutamate. In addition, Ba2+ was found to evoke glutamate release in the absence of K(+)-induced depolarization. Ba2+ (1-10 mM) depolarized synaptosomes, as measured by voltage-sensitive dye fluorescence and [3H]-tetraphenylphosphonium cation distribution. Ba2+ partially inhibited the increase in synaptosomal K+ efflux produced by depolarization, as reflected by the redistribution of radiolabeled 86Rb+. The release evoked by Ba2+ was inhibited by tetrodotoxin (TTX). Using the divalent cation indicator fura-2, cytosolic [Ca2+] increased during stimulation by approximately 200 nM, but cytosolic [Ba2+] increased by more than 1 microM. Taken together, our results indicate that Ba2+ initially depolarizes synaptosomes most likely by blocking a K+ channel, which then activates TTX-sensitive Na+ channels, causing further depolarization, and finally enters synaptosomes through voltage-sensitive Ca2+ channels to evoke neurotransmitter release directly. Though Ba(2+)-evoked glutamate release was comparable in level to that obtained with K(+)-induced depolarization in the presence of Ca2+, the apparent intrasynaptosomal level of Ba2+ required for a given amount of glutamate release was found to be several-fold higher than that required of Ca2+.
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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/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamates,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
61
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1220-30
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7690845-Animals,
pubmed-meshheading:7690845-Barium,
pubmed-meshheading:7690845-Brain,
pubmed-meshheading:7690845-Calcium Channels,
pubmed-meshheading:7690845-Electrophysiology,
pubmed-meshheading:7690845-Glutamates,
pubmed-meshheading:7690845-Glutamic Acid,
pubmed-meshheading:7690845-Intracellular Membranes,
pubmed-meshheading:7690845-Ion Channels,
pubmed-meshheading:7690845-Male,
pubmed-meshheading:7690845-Membrane Potentials,
pubmed-meshheading:7690845-Nerve Tissue Proteins,
pubmed-meshheading:7690845-Phosphorylation,
pubmed-meshheading:7690845-Potassium Channels,
pubmed-meshheading:7690845-Rats,
pubmed-meshheading:7690845-Sodium Channels,
pubmed-meshheading:7690845-Synaptosomes
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pubmed:year |
1993
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pubmed:articleTitle |
Barium evokes glutamate release from rat brain synaptosomes by membrane depolarization: involvement of K+, Na+, and Ca2+ channels.
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pubmed:affiliation |
Department of Pharmacology, Medical College of Pennsylvania, Philadelphia, Pennsylvania 19129.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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