Linked Life Data

7552261

Source:http://linkedlifedata.com/resource/pubmed/id/7552261

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-11-14
pubmed:abstractText
gamma-Aminobutyric acid (GABA) is normally primarily in amacrine cells in the rat retina. Immediately after an ischaemic insult, attained by occlusion of the central retinal artery for 60 min, GABA is then found to be associated with Müller cells. During subsequent reperfusion, the distribution of GABA immunoreactivity gradually reverts from the glial cells back into neuronal elements of the retina. Twenty-four hours after ischaemia, GABA staining is indistinguishable from that seen in control animals. It is suggested that during central retinal artery occlusion, Müller cell energy levels are sufficient to allow the active uptake of released GABA, but insufficient to metabolise it to glutamine. The normal cycle of GABA metabolites from Müller cells to neurones is thus inhibited. Restoration of blood flow and the consequent increase in retinal energy levels, as indicated by a slight recovery of the electroretinogram b-wave, facilitates glutamine shunting between glial cells and amacrine cells, resulting in the synthesis of neuronal GABA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
677
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Redistribution of GABA immunoreactivity following central retinal artery occlusion.
pubmed:affiliation
Nuffield Laboratory of Ophthalmology, University of Oxford, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't