The effects of alterations in the androgen status of male rats was investigated with respect to the possible involvement of hormones in GABAergic regulation. The methods used to study this hormone-GABA relationship revealed: 1. (1) Long term castration of rats caused a decrease in GABA concentration in the amygdala and septal area, while a slight but consistent increase in concentration was found in the midbrain. 2. (2) Testosterone substitution was effective in reversing this decrease in GABA associated with castration, but had no discriminable effect on the midbrain steady state concentrations. 3. (3) Estradiol substitution reversed the reduction in GABA found with castration and further increased GABA concentrations in the midbrain. 4. (4) Dihydrotestosterone had no effect on amygdaloid or septal concentrations but was effective in reducing GABA concentration in the midbrain. 5. (5) After GABA transaminase inhibition by aminooxyacetic acid the concentration of GABA in castrated animals was lower compared to sham animals in all 3 brain regions. Testosterone reversed this reduction in all areas. The findings suggest that castration causes a decrease in GABA synthesis in several brain regions and that this is an effect of a reduction in circulating testosterone and/or estradiol concentrations. Castration may also cause a decrease in turnover of GABA in the midbrain which is reversed by dihydrotestosterone and/or testosterone.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Oct 20 1978|
ASJC Scopus subject areas
- Molecular Biology
- Clinical Neurology
- Developmental Biology