Mechanism of the galanin induced increase in acetylcholine release in vivo from striata of freely moving rats.
Brain Res
; 589(1): 33-8, 1992 Aug 28.
Article
em En
| MEDLINE
| ID: mdl-1384927
ABSTRACT
Galanin (GAL) administered intracerebroventricularly (i.c.v.) induced a strong and long-lasting increase in the basal acetylcholine (ACh) release from striata of freely moving rats only when the excitatory corticostriatal input was removed, while its effect was transient in striata of sham-operated rats. This effect was dose-dependent (0.78, 1.56 and 3.12 nmol) and was completely prevented by the GAL receptor antagonist, galantide. GAL injected locally (3.12 nmol) in deafferented striata also induced a persistent increase in ACh release although to a lower extent. The impairment of monoaminergic neurotransmission caused by alpha-methylparatyrosine or p-chlorophenylalanine, respectively inhibitors of catecholamine and serotonin synthesis, completely prevented the rise in ACh output from deafferented striata while the muscarinic antagonist, scopolamine (0.5 mg/kg, s.c.), failed to do it. The data suggest that GAL in the deafferented striatum facilitates basal ACh release through an indirect mechanism. The effect seems to be at least partly mediated by an action of GAL on specific receptors in the striata.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Peptídeos
/
Neuropeptídeos
/
Acetilcolina
/
Corpo Estriado
/
Movimento
Limite:
Animals
Idioma:
En
Revista:
Brain Res
Ano de publicação:
1992
Tipo de documento:
Article
País de afiliação:
Itália