Document Detail

Changes in cholinergic but not in GABAergic markers in amygdala, piriform cortex, and nucleus basalis of the rat brain following systemic administration of kainic acid.
MedLine Citation:
PMID:  2542459     Owner:  NLM     Status:  MEDLINE    
Three days after systemic administration of kainic acid (15 mg/kg, s.c.), selected cholinergic markers (choline acetyltransferase, acetylcholinesterase, muscarinic acetylcholine receptor, and high-affinity choline uptake) and GABAergic parameters [benzodiazepine and gamma-aminobutyric acid (GABA) receptors] were studied in the frontal and piriform cortex, dorsal hippocampus, amygdaloid complex, and nucleus basalis. Kainic acid treatment resulted in a significant reduction of choline acetyltransferase activity in the piriform cortex (by 20%), amygdala (by 19%), and nucleus basalis (by 31%) in comparison with vehicle-injected control rats. A lower activity of acetylcholinesterase was also determined in the piriform cortex following parenteral kainic acid administration. [3H]Quinuclidinyl benzilate binding to muscarinic acetylcholine receptors was significantly decreased in the piriform cortex (by 33%), amygdala (by 39%), and nucleus basalis (by 33%) in the group treated with kainic acid, whereas such binding in the hippocampus and frontal cortex was not affected by kainic acid. Sodium-dependent high-affinity choline uptake into cholinergic nerve terminals was decreased in the piriform cortex (by 25%) and amygdala (by 24%) after kainic acid treatment. In contrast, [3H]flunitrazepam binding to benzodiazepine receptors and [3H]muscimol binding to GABA receptors were not affected 3 days after parenteral kainic acid application in any of the brain regions studied. The data indicate that kainic acid-induced limbic seizures result in a loss of cholinergic cells in the nucleus basalis that is paralleled by degeneration of cholinergic fibers and cholinoceptive structures in the piriform cortex and amygdala, a finding emphasizing the important role of cholinergic mechanisms in generating and/or maintaining seizure activity.
R Schliebs; M Zivin; J Steinbach; T Rothe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  53     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1989 Jul 
Date Detail:
Created Date:  1989-07-13     Completed Date:  1989-07-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  212-8     Citation Subset:  IM    
Paul Flechsig Institute for Brain Research, Department of Neurochemistry, Karl Marx University, Leipzig, G.D.R.
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MeSH Terms
Amygdala / metabolism
Basal Ganglia / metabolism*
Behavior, Animal / drug effects
Biological Markers / metabolism
Cerebral Cortex / metabolism
Kainic Acid / pharmacology*
Limbic System / metabolism*
Olfactory Pathways / metabolism
Parasympathetic Nervous System / metabolism*
Receptors, GABA-A / metabolism
Seizures / chemically induced
Substantia Innominata / metabolism*
gamma-Aminobutyric Acid / metabolism*
Reg. No./Substance:
0/Biological Markers; 0/Receptors, GABA-A; 487-79-6/Kainic Acid; 56-12-2/gamma-Aminobutyric Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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