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.

Article date: 1989/7/1

PubMed ID: 2542459

Journal name: Journal of neurochemistry (ISSN: 0022-3042)


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.

This document is available from: http://directlinks.cc/files/muscimol/2542459.pdf

Author List: Schliebs R, Zivin M, Steinbach J, Rothe T

Publication Types: Journal Article; Research Support, Non-U.S. Gov't

Substances mentioned in the article: Biomarkers; Receptors, GABA-A; gamma-Aminobutyric Acid; Kainic Acid;

Mesh terms: Amygdala/metabolism; Animals; Basal Ganglia/metabolism; Behavior, Animal/drug effects; Biomarkers/metabolism; Cerebral Cortex/metabolism; Kainic Acid/pharmacology; Limbic System/metabolism; Male; Olfactory Pathways/metabolism; Parasympathetic Nervous System/metabolism; Rats; Receptors, GABA-A/metabolism; Seizures/chemically induced; Substantia Innominata/metabolism; gamma-Aminobutyric Acid/metabolism;

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