Linked Life Data

2902196

Source:http://linkedlifedata.com/resource/pubmed/id/2902196

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1988-11-22
pubmed:abstractText
We have previously described a marked attenuation of postischemic striatal neuronal death by prior substantia nigra (SN) lesioning. The present study was carried out to evaluate whether the protective effect of the lesion involves changes in the degree of local cerebral blood flow (ICBF) reduction, energy metabolite depletion, or alterations in the extracellular release of striatal dopamine (DA), glutamate (Glu), or gamma-aminobutyric acid (GABA). Control and SN-lesioned rats were subjected to 20 min of forebrain ischemia by four-vessel occlusion combined with systemic hypotension. Levels of ICBF, as measured by the autoradiographic method, and energy metabolites were uniformly reduced in both the ipsi- and contralateral striata at the end of the ischemic period, a finding implying that the lesion did not affect the severity of the ischemic insult itself. Extracellular neurotransmitter levels were measured by microdialysis; the perfusate was collected before, during, and after ischemia. An approximately 500-fold increase in DA content, a 7-fold increase in Glu content, and a 5-fold increase in GABA content were observed during ischemia in nonlesioned animals. These levels gradually returned to baseline by 30 min of reperfusion. In SN-lesioned rats, the release of DA was completely prevented, the release of GABA was not affected, and the release of Glu was partially attenuated. However, excessive extracellular Glu concentrations were still attained, which are potentially toxic. This, taken together with the previous neuropathological findings, suggests that excessive release of DA is important for the development of ischemic cell damage in the striatum.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1455-64
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2902196-3,4-Dihydroxyphenylacetic Acid, pubmed-meshheading:2902196-Animals, pubmed-meshheading:2902196-Cerebrovascular Circulation, pubmed-meshheading:2902196-Corpus Striatum, pubmed-meshheading:2902196-Denervation, pubmed-meshheading:2902196-Dialysis, pubmed-meshheading:2902196-Dopamine, pubmed-meshheading:2902196-Energy Metabolism, pubmed-meshheading:2902196-Glutamates, pubmed-meshheading:2902196-Glutamic Acid, pubmed-meshheading:2902196-Homovanillic Acid, pubmed-meshheading:2902196-Hydroxydopamines, pubmed-meshheading:2902196-Ischemic Attack, Transient, pubmed-meshheading:2902196-Kinetics, pubmed-meshheading:2902196-Male, pubmed-meshheading:2902196-Oxidopamine, pubmed-meshheading:2902196-Rats, pubmed-meshheading:2902196-Rats, Inbred Strains, pubmed-meshheading:2902196-Substantia Nigra, pubmed-meshheading:2902196-gamma-Aminobutyric Acid
pubmed:year
1988
pubmed:articleTitle
Effect of ischemia on the in vivo release of striatal dopamine, glutamate, and gamma-aminobutyric acid studied by intracerebral microdialysis.
pubmed:affiliation
Department of Neurology, University of Miami School of Medicine, Florida 33101.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't