Linked Life Data

6138103

Source:http://linkedlifedata.com/resource/pubmed/id/6138103

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1983-12-17
pubmed:abstractText
Data of the inhibitory analysis suggest that the increase in the content of calcium in veratrine-, ouabain- and 80 mM K+-depolarized synaptosomes is due to Ca2+ influx through the potential-dependent calcium channels. The decrease of the intracellular concentration of Ca2+ in depolarized nerve endings is mainly caused by the calmodulin-dependent Ca,Mg-ATPase of synaptolemma and mitochondria. The regularities of ATP-dependent Ca2+ transport in synaptosomal plasma membranes were studied on the microsomes whose properties were found identical to those of native synaptolemma. A comparison of the kinetic parameters of Ca-transport systems in brain microsomes and mitochondria and the data on extensive inhibition of 45Ca uptake by rotenone and oligomycin suggest that mitochondria play a key role in the control of intraterminal concentration of Ca2+ during nerve impulse conduction.
pubmed:language
rus
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0320-9725
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1249-55
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
[Mechanisms of calcium transport in brain synaptosomes as affected by depolarization].
pubmed:publicationType
Journal Article, English Abstract