Further evidence for abnormal GABAergic circuits in amygdala-kindled rats.

Article date: 1987/9/15

PubMed ID: 2823978

Journal name: Brain research (ISSN: 0006-8993)


In amygdala-kindled rats, synaptosomal levels of gamma-aminobutyric acid (GABA) and its synthesizing enzyme glutamate decarboxylase as well as [3H]GABA binding to synaptic membranes were determined in several brain regions which, except for the amygdala, were pooled from both hemispheres to obtain enough tissue for the subcellular fractionations. Compared to controls, GABA synthesis was reduced in the ipsilateral (stimulated) amygdala and in corpus striatum and substantia nigra. GABA receptor binding was decreased in amygdala and substantia nigra but significantly increased in the striatum. The data suggest that abnormal GABAergic transmission in discrete brain areas may be involved in the generation and propagation of amygdala-kindled seizures.

This document is available from: http://directlinks.cc/files/muscimol/2823978.pdf

Author List: Löscher W, Schwark W S

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

Substances mentioned in the article: Receptors, GABA-A; Muscimol; gamma-Aminobutyric Acid; Glutamate Decarboxylase;

Mesh terms: Amygdala/physiopathology; Animals; Brain/metabolism; Female; Glutamate Decarboxylase/metabolism; Kindling, Neurologic; Muscimol/metabolism; Rats; Rats, Inbred Strains; Receptors, GABA-A/metabolism; Synaptosomes/metabolism; gamma-Aminobutyric Acid/metabolism;

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