Hypothalamic responsiveness during lactation in the rat: Luteinizing hormone release after electrochemical stimulation

To assess the ability of the hypothalamus to release gonadotropin releasing hormone (GnRH) during lactation, electrochemical (EC) stimulation of the medial preoptic area (MPOA) was performed by passing 100 μAmps DC for 60 sec. In females nursing 8 pups, EC stimulation on Days 5 or 10 postpartum caused an increase in luteinizing hormone (LH) which was only slightly less than the response observed during diestrus-1 (D-1) of the estrous cycle. In females nursing 2 pups, or in females deprived of their 8-pup litters for 24 or 48 h, EC stimulation resulted in a much greater LH response than observed in females during D-1. Basal LH concentrations measured before EC stimulation averaged 20-40 ng/ml in females during D-1, females nursing 2 pups, and females deprived of their litters for 24 or 48 h, compared with concentrations <10 ng/ml in females nursing 8 pups. To determine whether decreased GnRH secretion could account for the smaller estrogen-induced LH surges observed during lactation, EC stimulation was performed on Day 10 postpartum, using ovariectomized, estrogen-progesterone treated animals in which the endogenous LH surges were blocked with sodium pentobarbital. The results showed that the presence of the 8-pup litters greatly decreased the peak LH responses after EC stimulation when compared with nonlactating animals. Additional studies were performed to determine the site of action of prolactin in suppressing the postcastration rise in LH. Pituitary responsiveness to GnRH and LH release after EC stimulation of the MPOA were determined on Day 8 postpartum, or 5 days after ovariectomy. One group of animals nursing 8 pups received 1 mg ergocryptine daily to block suckling-induced prolactin secretion. LH levels in the control females nursing 8 pups showed no postcastration rise on Day 8, whereas inhibition of prolactin secretion in the continued presence of suckling led to a significant postcastration response (<10 ng/ml vs. 70-90 ng/ml). Administration of 500 ng GnRH to the control and ergocryptine-treated animals yielded similar peak LH responses, suggesting that the site of action of prolactin in suppressing LH must be at the central nervous system, (CNS). EC stimulation of the MPOA of the suckled animals resulted in significantly greater peak LH responses in the absence of prolactin than in the presence of prolactin. These results suggest that the suppression of basal LH secretion during lactation is due primarily to diminished GnRH secretion. Furthermore, the elevated levels of prolactin during lactation may be acting on the hypothalamus to suppress GnRH secretion.