Linked Life Data

7350970

Source:http://linkedlifedata.com/resource/pubmed/id/7350970

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1980-3-17
pubmed:abstractText
It is known that transmitter release depends upon the entry of calcium ions into the synaptic terminal. Mitochondria have been suggested to play a key role on the regulation of intracellular Ca2+ concentration, thereby influencing transmitter liberation and synaptic transmission. Here we report the stimulatory effect of DNP and FCCP, uncouplers of oxidative phosphorylation, and quinidine, known to induce muscle contractures and increase Ca2+ efflux from muscle mitochondria, on both [14C]glutamic acid and [3H]GABA unstimulated release from synaptosomes and loss of 45Ca2+ from preloaded whole brain mitochondria. Results showed that the spontaneous efflux of non-putative neurotransmitters, leucine and alpha-aminoisobutyric acid, was less affected or not stimulated at all, under similar experimental conditions. Data suggest that calcium ions released from mitochondria are able to trigger neurotransmitter release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
181
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
357-67
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Studies on the relationship between Ca2+ efflux from mitochondria and the release of amino acid neurotransmitters.
pubmed:publicationType
Journal Article