Intracisternal administration of synthetic human β-endorphin in rats increased plasma prolactin. This effect of β-endorphin is blocked completely by parenteral administration of the dopamine receptor agonist, apomorphine. Increasing availability of brain dopamine with the monoamine oxidase inhibitor, pargyline, blunted the effect of β-endorphin on plasma prolactin. Although the effect of apomorphine could have been mediated either in the hypothalamus or directly on pituitary, the action of pargyline could not have occurred in pituitary, thus providing support for the hypothesis that β-endorphin-induced prolactin secretion is mediated in brain and furthermore through a dopaminergic mechanism. Additional support for both aspects of this hypothesis is provided by the finding that decreasing availability of dopamine with the dopamine synthesis inhibitor, α-methyltyrosine, potentiated the effect of β-endorphin to increase plasma prolactin concentration.Furthermore, this potentiation by α-methyltyrosine of β-endorphin-induced prolactin secretion was evident at a time when mediobasal hypothalamic dopamine concentration had not yet decreased. Because the storage pool of dopamine does not appear to have been altered at this time, these data suggest that lack of newly synthesized hypothalamic dopamine potentiated the effect of β-endorphin to increase plasma prolactin. It seems probable that inhibition of release of newly synthesized (and preferentially released) tuberoinfundibular dopamine is important in mediating β-endorphin-induced prolactin secretion. Finally, intracisternal dexamethasone inhibited the synergistic effects of α-methyltyrosine and β-endorphin on prolactin secretion, perhaps by an action on hypothalamic aminergic neurons.
Hypothalamic dopamine signalling regulates brown fat thermogenesis