Linked Life Data

7477952

Source:http://linkedlifedata.com/resource/pubmed/id/7477952

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-12-12
pubmed:abstractText
The effects of maximal electroshock, used as a model of generalized seizures, were studied on extracellular GABA and glutamate levels in the ventral hippocampus of the freely-moving rat, using in vivo microdialysis. Following a maximal electroshock there was a rapid decline in GABA levels (46 +/- 5%) in the 20 min immediately after the seizure and levels remained depressed for a further 60 min. However, although there was a transient small decrease (11 +/- 2%) in glutamate levels in the first 20 min post-ictally, there followed a more prolonged, larger increase in the next 40 min. Maximal electroshock, administered in the absence of extracellular calcium, did not change GABA levels, while glutamate levels were again increased (42 +/- 8%) in the 40-80 min after the shock. Local perfusion with nickel (1 mM) to block T-type calcium channels had no effect on basal GABA or glutamate levels but prevented maximal electroshock-induced changes in both amino acids. Experiments were carried out to test the hypothesis that the post-ictal increased glutamate release was due to the decrease in GABA release. Perfusion with the potent GABA re-uptake inhibitor NNC-711, for 60 min prior to administration of maximal electroshock, increased GABA levels (436 +/- 58%) and abolished the seizure-induced decrease. Basal glutamate levels were not affected by perfusion with NNC-711 but subsequent maximal electroshock also failed to affect levels. Local perfusion with the GABAA receptor antagonist bicuculline (1, 10 and 100 microM) had no effect on basal GABA levels but glutamate levels were increased (46 +/- 5%) after perfusion with 100 microM bicuculline.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
415-22
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7477952-Amino Acids, pubmed-meshheading:7477952-Animals, pubmed-meshheading:7477952-Anticonvulsants, pubmed-meshheading:7477952-Bicuculline, pubmed-meshheading:7477952-Calcium, pubmed-meshheading:7477952-Electroshock, pubmed-meshheading:7477952-Epilepsy, Tonic-Clonic, pubmed-meshheading:7477952-Extracellular Space, pubmed-meshheading:7477952-GABA Antagonists, pubmed-meshheading:7477952-Glutamic Acid, pubmed-meshheading:7477952-Hippocampus, pubmed-meshheading:7477952-Male, pubmed-meshheading:7477952-Microdialysis, pubmed-meshheading:7477952-Nickel, pubmed-meshheading:7477952-Nicotinic Acids, pubmed-meshheading:7477952-Nipecotic Acids, pubmed-meshheading:7477952-Oximes, pubmed-meshheading:7477952-Rats, pubmed-meshheading:7477952-Synaptic Transmission, pubmed-meshheading:7477952-gamma-Aminobutyric Acid
pubmed:year
1995
pubmed:articleTitle
Decreased GABA release following tonic-clonic seizures is associated with an increase in extracellular glutamate in rat hippocampus in vivo.
pubmed:affiliation
Department of Physiology and Pharmacology, University of Nottingham Medical School, Queen's Medical Centre, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't