The role of prolactin and of estradiol and progesterone in the control of the biosynthetic and secretory activity of TIDA neurons has been investigated in the following animal models: young female rats, aged female rats, and young male rats. The indices of TIDA neuronal function employed were a) mass of TH in neurites in the ME, b) total in situ activity of TH in the ME, c) in situ molar activity of TH in the ME, and d) secretion of dopamine into hypophysial portal blood. It was found that prolactin in high concentration in the circulation and in the CSF had little, if any, effect on the mass of TH in the ME. However, a high concentration of prolactin in either the circulation or in the CSF stimulated significantly the in situ TH activity in the ME whether expressed in terms of total activity per ME or activity per mole of TH. The stimulation of TH activity with prolactin was prevented by immunoneutralization of circulating prolactin. A high concentration of prolactin in the CSF was as effective in stimulating TH activity in the ME of rats with intact pituitary glands as in hypophysectomized rats. In addition to prolactin, treatment of animals with intact pituitaries with a combination of estradiol and progesterone markedly stimulated the total in situ activity of TH of the ME as well as the in situ molar activity of TH of the ME, but neither estradiol nor progesterone alone had an effect on TH activity. Hypophysectomy abolished the stimulatory action of estradiol and progesterone on TH activity of the ME. In addition to the in situ activity of TH in the ME, estradiol-progesterone treatment stimulated the secretion of dopamine into hypophysial portal blood. Neither estradiol nor progesterone alone affected dopamine secretion by TIDA neurons. We conclude that exposure to high concentrations of prolactin or to both estradiol and progesterone stimulate the biosynthetic and secretory activity of TIDA neurons. These hormones are effective in old rats and well as young rats and in males as well as females.