Prolactin release following electrical stimulation of the brain in ovarectomized and ovariectomized estrogen-treated rhesus monkeys.

Selected areas in the medial basal (MBH) and rostral (RH) hypothalamus and in the amygdala (AMYG) of long-term ovariectomized rhesus monkeys were electrically stimulated for 30 min through permanently implanted bilateral stainless steel electrodes. Stimulation of an area in the MBH extending from the dorsal part of the ventromedial nucleus through the arcurate nucleus to the upper median eminence resulted in a 200 to 400% increase within 5 min in 8 monkeys. In one monkey the elevated serum prolactin levels persisted after termination of stimulation and in 2 monkeys prolactin remained unchanged during the 30-min stimulation but increased after stimulation was discontinued. Stimulation of the paraventricular-dorsomedial nuclear area in one monkey had no effect on prolactin release. Prolactin responses to stimulation in the RH varied. In 2 monkeys the electrode tips extended into the optic chiasm but part of the uninsulated tips remained in contact with the RH; only one of these monkeys released prolactin in response to stimulation. In 4 monkeys the electrode tips were located in the suprachiasmatic-anterior hypothalamus area. Serum prolactin increased by 200 to 300% in response to stimulation in 2 of these monkeys but increased only slightly in the remaining 2 monkeys. Prolactin responses to stimulation of the AMYG varied with the location of the electrodes. Stimulation in the corticomedial region produced no change in serum prolactin but stimulation in the basal or basolateral area produced marked elevations. An increase in circulating levels of estradiol-17beta (E2) to 100 pg/ml by SC implantation of E2 capsules 72 h before stimulation had no significant effect on basal prolactin levels, but markedly enhanced the prolactin release induced by stimulation in both the MBH and RH. Sham-stimulation did not affect serum prolactin. We conclude that prolactin release in rhesus monkeys can be triggered by electrical stimulation of selected hypothalamic and amygdaloid areas and that stimulation-induced prolactin release in the RH and MBH can be enhanced by E2 pretreatment.