The effects of diclofensine, a pure dopamine (DA) uptake inhibitor on 1) 3H-DA uptake in rat arcuate-periventricular nucleus-median eminence synaptosomes, 2) basal and K+-evoked endogenous DA release from tuberoinfundibular dopaminergic (TIDA) neurons and 3) in vivo prolactin (PRL) secretion were studied. Diclofensine, in concentrations of 0.01, 0.1 and 1 microM caused a marked decrease of 3H-DA uptake. In addition, it was unable to stimulate basal endogenous DA release which, on the contrary, was elicited by d-amphetamine in the same concentration (50 microM). On the other hand, diclofensine (50 microM) caused a 3 fold enhancement of K+-evoked DA release. Finally, the compound, when administered in vivo to male rats, significantly reduced basal serum PRL levels. The results of the present study seem to indicate that the pharmacological blockade of DA uptake in TIDA neurons is a condition sufficient to cause a reduction of PRL release.
Pure uptake blockers of dopamine can reduce prolactin secretion: studies with diclofensine / DI RENZO, GIANFRANCO MARIA LUIGI; S., Amoroso; Taglialatela, Maurizio; Lm, Canzoniero; P., Maida; Lombardi, Gaetano; Annunziato, Lucio. - In: LIFE SCIENCES. - ISSN 0024-3205. - ELETTRONICO. - 42:(1988), pp. 2161-2169.
Pure uptake blockers of dopamine can reduce prolactin secretion: studies with diclofensine
DI RENZO, GIANFRANCO MARIA LUIGI;TAGLIALATELA, MAURIZIO;LOMBARDI, GAETANO;ANNUNZIATO, LUCIO
1988
Abstract
The effects of diclofensine, a pure dopamine (DA) uptake inhibitor on 1) 3H-DA uptake in rat arcuate-periventricular nucleus-median eminence synaptosomes, 2) basal and K+-evoked endogenous DA release from tuberoinfundibular dopaminergic (TIDA) neurons and 3) in vivo prolactin (PRL) secretion were studied. Diclofensine, in concentrations of 0.01, 0.1 and 1 microM caused a marked decrease of 3H-DA uptake. In addition, it was unable to stimulate basal endogenous DA release which, on the contrary, was elicited by d-amphetamine in the same concentration (50 microM). On the other hand, diclofensine (50 microM) caused a 3 fold enhancement of K+-evoked DA release. Finally, the compound, when administered in vivo to male rats, significantly reduced basal serum PRL levels. The results of the present study seem to indicate that the pharmacological blockade of DA uptake in TIDA neurons is a condition sufficient to cause a reduction of PRL release.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
