Linked Life Data

9771130

Source:http://linkedlifedata.com/resource/pubmed/id/9771130

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1998-12-1
pubmed:abstractText
The present paper summarizes the data obtained in studying the mechanisms of glutamate-induced deterioration of neuronal Ca2+ homeostasis. In the cultured mammalian central neurons, a short-term (< 1 min) glutamate (GLU, 100 mu) challenge is known to induce a readily reversible (transient) neuronal [Ca2+]i increase. In contrast, a long-term (15-30 min) GLU exposure leads to the appearance of high [Ca2+]i plateau or to the partial recovery of the increased [Ca2+]i. Experiments show that impaired [Ca2+]i recovery in the postglutamate period cannot be explained by the increased [Ca2+]i permeability of the neuronal membrane, as earlier considered. Moreover, a sustained elevation of [Ca2+]i during and after chronic GLU application is associated with a progressive decrease in Ca2+ permeability. The major cause of GLU-induced Ca2+ overload is the mitochondrial depolarization resulted from excessive Ca2+ influx into the mitochondria, the generation of free radicals and the opening of a "giant pore" in the inner mitochondrial membrane. This in turn suppresses both ATP synthesis and Ca2+ electrophoretic uptake into the mitochondrial matrix. In combination with [Ca2+]i-dependent acidification, this leads to the suppression of Ca2+ release from the cell via Na+/Ca2+ exchanger and Ca2+/H+ pump of the neuronal membrane. Therefore, [Ca2+]i recovery following a long-term GLU treatment becomes strongly or even irreversibly compromised.
pubmed:language
rus
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0869-6047
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
41-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
[Mechanisms of neuronal calcium homeostasis destabilization caused by hyperstimulation of glutamate receptors].
pubmed:publicationType
Journal Article, Comparative Study, English Abstract