Linked Life Data

9416769

Source:http://linkedlifedata.com/resource/pubmed/id/9416769

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25
pubmed:dateCreated
1998-1-14
pubmed:abstractText
CNS glutamatergic transmission is altered by chronic ethanol intake and may underlie the behavioral hyperactivity associated with ethanol withdrawal. Because astrocytes regulate extracellular glutamate levels, the aim of this investigation was to characterize the effects of in vitro ethanol exposure on Na+-dependent glutamate uptake parameters in astrocytes. Ethanol exposure elicited a time and concentration-dependent increase in the maximal uptake capacity, Vmax, for [3H] glutamate, which was reversed upon withdrawal of ethanol from the media. None of the ethanol exposures had any effect on the Km for this process. In addition, the ethanol-induced increase in Vmax for glutamate was reversed by the protein kinase C inhibitors, calphostin C and bisindolylmaleimide, and was not associated with an increase in the expression of either of the major glutamate transporter proteins, GLT-1 or GLAST.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2499-505
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Regulation of glutamate uptake in astrocytes continuously exposed to ethanol.
pubmed:affiliation
Department of Veterans Affairs Medical Center and The Department of Pharmacology, University of Arizona, Tucson 85724, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.