Abstract

The acute effects of corticosterone (0.5 and 1 mg/kg, i.p.) upon the GABAergic system have been investigated. While no changes were detected after treatment with corticosterone 0.5 mg/kg, the administration of 1 mg/kg lowered the levels of gamma-aminobutyric acid (GABA) (29%) in the mediobasal hypothalamus either 30 or 60 min after injection in both young (3-4 weeks old) and adult (7-8 weeks old) rats. No changes were found in the frontal cerebral cortex. Only in young rats did the administration of corticosterone (1 mg/kg, 30 min) reduced GABA levels in the corpus striatum (34%). In young rats this dose of corticosterone: 1. did not affect the activity of the enzymes of the metabolism of GABA (GAD and GABA-T); 2. reduced neuronal 3H-GABA uptake in the corpus striatum (30%) and in the mediobasal hypothalamus (46%), and increased it in the frontal cortex (2-fold); 3. enhanced the turnover of GABA (2-fold) in the corpus striatum. These values were unaffected by 0.5 mg/kg. Corticosterone 0.5 and 1 mg/kg did not alter non-neuronal 3H-GABA uptake. These findings show an area-related and age- and dose-dependent response of the GABAergic pathways to acute corticosterone treatment. This is discussed in relation to the age-related sensitivity to the environmental stimuli which cause this release of corticosteroids. The stimulation of GABAergic function which occurs mainly in the corpus striatum as estimated from the increase in its turnover may be related to the postulated anticonvulsant role of corticosteroids.

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