Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-12-6
pubmed:abstractText
Some aspects of the GABA and cholinergic systems have been investigated in the cortex and thalamus of GAERS Wistar rats, a model of petit-mal epilepsy, and in a non-epileptic control strain. GABA and its synthetic enzyme, glutamic acid decarboxylase (GAD), were located by immunocytochemistry; the GABAA receptors were evaluated by autoradiography of GABA-enhanced 3H-flunitrazepam binding and by immunocytochemistry using specific antibodies against the beta 2-beta 3 subunits of GABAA receptor protein. GABA and GAD immunocytochemistry did not show up any difference in density or distribution of immunoreactive elements (fibers, terminals and neurons) between epileptic and control animals, but autoradiographic and immunocytochemical studies showed a decreased enhancement of 3H-flunitrazepam binding and of beta 2-beta 3 subunits of GABAA receptor in the sensorimotor cortex and anterior thalamic areas of the epileptic strain. No differences were found in benzodiazepine receptors in the two strains. GABAB receptors were measured as 3H-baclofen binding in a crude synaptic membrane preparation and there was no difference between epileptic and control animals. Choline acetyltransferase, the synthetic enzyme for acetylcholine, and muscarinic receptor subtypes (M1 and M2), visualized respectively by an immunocytochemical procedure and binding autoradiography, did not differ in epileptic and normal rats. The data suggest an impairment of the 'GABAA system' in restricted brain regions of epileptic rats, due to a reduction of receptor beta 2-beta 3 subunits and coupling to benzodiazepine receptors despite the normal synthesis and location of the neurotransmitter.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0920-1211
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
229-38
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8223419-Acetylcholine, pubmed-meshheading:8223419-Animals, pubmed-meshheading:8223419-Autoradiography, pubmed-meshheading:8223419-Cerebral Cortex, pubmed-meshheading:8223419-Choline O-Acetyltransferase, pubmed-meshheading:8223419-Epilepsy, Absence, pubmed-meshheading:8223419-Flunitrazepam, pubmed-meshheading:8223419-Glutamate Decarboxylase, pubmed-meshheading:8223419-Immunohistochemistry, pubmed-meshheading:8223419-Male, pubmed-meshheading:8223419-Radioligand Assay, pubmed-meshheading:8223419-Rats, pubmed-meshheading:8223419-Rats, Wistar, pubmed-meshheading:8223419-Receptors, GABA-A, pubmed-meshheading:8223419-Receptors, GABA-B, pubmed-meshheading:8223419-Receptors, Muscarinic, pubmed-meshheading:8223419-Species Specificity, pubmed-meshheading:8223419-Synaptic Membranes, pubmed-meshheading:8223419-Thalamus
pubmed:year
1993
pubmed:articleTitle
GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS): an immunocytochemical and receptor binding autoradiographic study.
pubmed:affiliation
Dept. of Neurophysiology, Istituto Neurologico C. Besta, Milan, Italy.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't