ProB. Neuro-Psychopharrnocol & Biol. Psychiat. 1982, Vol. 6, pp. 355-358 0278-58461821060355-04503,0010 Printed in Great Britain. All rights reserved. CopyriRht © 1982 PerRamonPress Ltd. STIMI]LATORY CONTROL OF PROLACTIN BY DOPAMINE GREGORYM. BROWN and JO A. SEGGIE Departments of Neurosciences and Psychiatry McMaster University, Hamilton, Ontario, Canada (Final form, June 1982) Abstract Brown, Gregory M. and Jo A. Seggie: Stimulatory control of prolactin by dopamine. Prog. Neuro-Psychopharmacol. & Biol. Psychiat. 1982, 6(4-6) : 355-358. I. In addition to evidence that dopamine (DA) inhibits prolactin (PRL) via the tuberinfund- ibular system, there is also evidence for excitatory effects of DA via that system as well as evidence for regulation by DA sites lying behind the blood brain barrier. 2. Apomorphine (APO) was given to rats pretreated with either a peripheral (domperidone, DOM) or a central (haloperidol, HAL) DA blocker and prolactin responses examined. 3. Both DOM and HAL caused prolactin elevation. 4. Further elevation of prolactin was produced by APO in HAL treated animals, indicating an excitatory dopamine effect on prolactin. Keywords: prolactin, haloperidol, domperidone, apomorphine, dopamine. Abbreviations: prolactin (PRL), haloperidol (HAL), domperidone (DOM), apomorphine (APO), dopamine (DA). Introduction There is considerable evidence that dopamine regulation of prolactin is mediated via the tuberoinfundibular dopamine system. In a variety of studies dopamine agonists and antag- onists which are incapable of crossing the blood brain barrier have profound effects on prolactin release. Thus, administration of carbidopa, a peripheral L-aminoacid decarboxy- lase inhibitor which will prevent peripheral synthesis of dopamine causes an elevation in prolactin (Brown et al., 1976a). In contrast administration of dopamine itself causes a lowering of prolactin levels (LeBlanc et al., 1976) and administration of domperidone an agent which blocks dopamine receptors, produces a rise in prolactin (Brown et al., ). There is also evidence that these effects may be mediated by a direct action on the pit- uitary. Dopaminewill cause inhibition of prolactin release in vitro (Quijada et al., 1973/74). Dopamine infusion into the portal vessels will produce a lowering in prolactin (Takahara et al., 1974). Dopaminecan be measured in the portal vessels in concentrations sufficient to have effects on the pituitary (Ben-Jonathan et al., 1977) and stereospecific dopamine/neuroleptic receptors have been found in the pituitary (Brown et al., 1976b). On the basis of this evidence it is reasonable to conclude that the tuberioinfundibular dopamine may act as a physiologic prolactin inhibiting factor and that this effect is mediated, at least in part, by an action on the pituitary dopamine receptors. In addition to the foregoing there are studies indicating that DA systems lying behind the blood brain barrier may participate in prolactin regulation (Quijada et al., 1973/74; Szabo et al., 1977). Furthermore, excitatory effects on PRL release have been reported (Denet et al., 1980; Besser et al., 1981). In the present study we examined effects of APO on PRL release in the presence of block- ade by a peripheral (DOM) and a central (HAL) dopamine antagonist. 355