Further evidence for abnormal GABAergic circuits in amygdala-kindled rats.
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.
Löscher
W
W
Laboratory of Pharmacology and Toxicology, School of Veterinary Medicine, Free University of Berlin (F.R.G.).
Schwark
W S
WS
D000679:Amygdala / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D007696:Kindling, Neurologic; D009118:Muscimol / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D011963:Receptors, GABA-A; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase