INTERACTION OF OPIOID PEPTIDE-CONTAINING TERMINALS WITH DOPAMINERGIC PERIKARYA IN THE RAT HYPOTHALAMUS

Both direct pituitary and indirect CNS mechanisms have been postulated for the influence of opiate agonists on prolactin secretion. By examining the interactions between terminals of neurons containing opioid peptides and hypothalamic TH-positive cell bodies, this paper addressed the anatomical basis for the latter mechanism. Initial electron microscopic studies directly demonstrated contact between opioid peptide terminals and dopaminergic cell bodies and provided some visual criteria for assessing opioid-dopamine interactions at the light microscopic level. Using these guidelines, we examined the rates of contact on both A12 and A14 neurons of each of the three opioid peptide families: pro-enkephalin, pro-dynorphin, and pro-opiomelanocortin (POMC). For A14 neurons, many of which project to the posterior pituitary, contact rates were estimated at 15, 20, and 5% for dynorphin, Met-enkephalin, and ACTH (a POMC derivative), respectively. In contrast, the A12 dopamine neurons, which regulate prolactin secretion by inhibition, showed a roughly 70% contact rate with dynorphin axons (P < 0.001) with Met-enkephalin and ACTH contact rates remaining low at 20 and 5% respectively. Contact frequency varied significantly during the estrus cycle only with dynorphin contacts on A12 neurons. Proestrus and diestrus (less so) showed a small but significant (P < 0.05) elevation in contact rates versus estrus, male, lactating and pregnant groups. No other significant difference emerged among these groups. On the basis of these observations, we conclude that dynorphin represents a significant and specific factor in the innervation of A12 dopamine neurons. This relationship may account for some if not most of the influence of opiate agonists and antagonists on prolactin secretion.