Raphe 5-HT1A autoreceptors, but not postsynaptic 5-HT1A receptors or beta-adrenoceptors, restrain the citalopram-induced increase in extracellular 5-hydroxytryptamine in vivo.
Eur J Pharmacol
; 316(1): 43-7, 1996 Nov 28.
Article
en En
| MEDLINE
| ID: mdl-8982649
ABSTRACT
In vivo microdialysis in rat ventral hippocampus was used (i) to verify the importance of 5-HT1A autoreceptors in the raphe as targets for drugs that enhance the citalopram-induced elevation of forebrain 5-hydroxytryptamine (5-HT), and (ii) to further examine the specificity of (-)-penbutolol in this regard. The selective 5-HT1A receptor antagonist WAY100635 (s.c., or intra-raphe) or the mixed 5-HT1A/1B/beta-adrenoceptor antagonist (-)-penbutolol (s.c.), potentiated the citalopram-induced 5-HT rise, whereas local "reverse' dialysis of WAY100635 into the ventral hippocampus did not. Furthermore, the (-)-penbutolol-induced augmentation proved stereoselective and not mediated by beta-adrenoceptors (no effect of s.c. (+)-penbutolol, or beta 1- and beta 2-adrenoceptor blockers (betaxolol, ICI118.551)). These data provide direct evidence that increased stimulation of 5-HT1A autoreceptors in the midbrain raphe impedes the effect of citalopram on forebrain extracellular 5-HT, whereas neither postsynaptic 5-HT1A receptors nor beta-adrenoceptors appear to be involved.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Núcleos del Rafe
/
Citalopram
/
Serotonina
/
Receptores de Serotonina
/
Receptores Adrenérgicos beta
/
Inhibidores Selectivos de la Recaptación de Serotonina
Límite:
Animals
Idioma:
En
Revista:
Eur J Pharmacol
Año:
1996
Tipo del documento:
Article
País de afiliación:
Suecia