Steroid regulation of tyrosine hydroxylase messenger ribonucleic acid in dopaminergic subpopulations of monkey hypothalamus

PRL release in primates can be stimulated by progesterone (P) after estrogen (E) priming. Hypothalamic dopaminergic neurons are a primary inhibitory system of PRL secretion, which differentially express progestin receptors (PR) in a cell-specific manner. Thus, these neurons may be an important target of P for increasing PRL. To further this hypothesis, two studies were performed. First, verification of the subpopulations of dopaminergic neurons that express PR was obtained with a combination of immunocytochemistry for PR and in situ hybridization for tyrosine hydroxylase (TH). Second, the effects of E and E plus P on the expression of TH messenger RNA (mRNA) were examined with in situ hybridization and image analysis in five different subpopulations of dopaminergic neurons. In the first study, dual labeled neurons were found rostrally around the ventral portion of the third ventricle and in more caudal periventricular areas, including the dorsal arcuate nucleus. Little or no PR were observed in TH-positive neurons located in the lateral chiasmatic area, paraventricular nucleus, ventral arcuate nucleus, or the substantia nigra. These results are consistent with our previous observations using double immunocytochemistry. In the second study, there was no significant effect of E or E plus P on single cell levels of TH mRNA in dopaminergic neurons of the subventricular area, periventricular area, or paraventricular nucleus. However, E plus P treatment produced a significant decrease in TH mRNA in the ventral arcuate dopaminergic neurons. There was no effect of E or E plus P in the dorsal arcuate dopaminergic neurons. In conclusion, E plus P decreases the expression of TH mRNA in the ventral arcuate dopaminergic neurons, a subpopulation that rarely expresses PR. The decrease in TH mRNA in the ventral arcuate dopaminergic neurons after E and P treatment is consistent with a role for this subpopulation of tuberoinfundibular neurons in P-induced PRL secretion.