Clonidine differentially modulates the release of endogenous GABA in various rat brain areas.
Pharmacol Res
; 24(2): 189-96, 1991 Aug.
Article
em En
| MEDLINE
| ID: mdl-1749748
ABSTRACT
The effects of clonidine on the release of endogenous gamma-aminobutyric acid (GABA) have been studied in superfused synaptosomes prepared from rat hypothalamus, nucleus tractus solitarii (NTS) and cerebellum. Clonidine enhanced in a concentration-dependent manner the basal release of GABA from hypothalamus and NTS synaptosomes. In contrast, the imidazoline did not affect the release of the amino acid from the cerebellar preparation. The alpha 2-adrenoceptor antagonist yohimbine prevented the releasing effect of clonidine, while the alpha 1-adrenoceptor antagonist prazosin was ineffective. The results show that the release of GABA from hypothalamus or NTS nerve endings can be enhanced by clonidine through the activation of adrenoceptors of the alpha 2 subtype. The GABAergic nerve terminals of cerebellum do not seem to possess presynaptic adrenoceptors by which clonidine can regulate the basal outflow of the amino acid. The results suggest that some of the clonidine effects may occur through activation of the GABA system.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Química Encefálica
/
Clonidina
/
Ácido gama-Aminobutírico
Limite:
Animals
Idioma:
En
Revista:
Pharmacol Res
Assunto da revista:
FARMACOLOGIA
Ano de publicação:
1991
Tipo de documento:
Article
País de afiliação:
Itália