STEROID REGULATION OF TYROSINE-HYDROXYLASE MESSENGER-RIBONUCLEIC-ACIDIN DOPAMINERGIC SUBPOPULATIONS OF MONKEY HYPOTHALAMUS

PRL release in primates can be stimulated by progesterone (P) after es trogen (E) priming. Hypothalamic dopaminergic neurons are a primary in hibitory system of PRL secretion, which differentially express progest in receptors (PR) in a cell-specific manner. Thus, these neurons may b e an important target of P for increasing PRL. To further this hypothe sis, two studies were performed. First, verification of the subpopulat ions of dopaminergic neurons that express PR was obtained with a combi nation of immunocytochemistry for PR and in situ hybridization for tyr osine hydroxylase (TH). Second, the effects of E and E plus P on the e xpression of TH messenger RNA (mRNA) were examined with in situ hybrid ization and image analysis in five different subpopulations of dopamin ergic neurons. In the first study, dual labeled neurons were found ros trally around the ventral portion of the third ventricle and in more c audal periventricular areas, including the dorsal arcuate nucleus. Lit tle or no PR were observed in TH-positive neurons located in the later al chiasmatic area, paraven tricular nucleus, ventral arcuate nucleus, or the substantia nigra. These results are consistent with our previo us observations using double immunocytochemistry. In the second study, there was no significant effect of E or E plus P on single cell level s of TH mRNA in dopaminergic neurons of the subventricular area, periv entricular area, or paraventricular nucleus. However, E plus P treatme nt produced a significant decrease in TH mRNA in the ventral arcuate d opaminergic neurons. There was no effect of E or E plus P in the dorsa l arcuate dopaminergic neurons. In conclusion, E plus P decreases the expression of TH mRNA in the ventral arcuate dopaminergic neurons, a s ubpopulation that rarely expresses PR. The decrease in TH mRNA in the ventral arcuate dopaminergic neurons after E and P treatment is consis tent with a role for this subpopulation of tuberoinfundibular neurons in P-induced PRL secretion.