Progesterone and corticosteroid regulation of hypothalamic and pituitary opioid content during LH surge induction

The purpose of this study was to determine whether steroid hormones affect brain opioid content during the time of gonadotropin surge induction. Ovariectomized rats (26 days old) were primed with estradiol (E(2)) (2 mug) for 2 days. E(2) treatment markedly suppressed hypothalamic beta-endorphin content at 1500 h, 1800 h (Day 29), and 0800 h (Day 30) but had no effect on pituitary beta-endorphin levels. The administration of progesterone (P(4)) at 0900 h on Day 29 caused a luteinizing hormone (LH) and a follicle-stimulating hormone (FSH) surge at 1500 h that same day. Interestingly, hypothalamic beta-endorphin content was unchanged during the LH surge induced by P(4), although a nonsignificant elevation of hypothalamic beta-endorphin levels was noticed in P(4)-treated rats the morning after the surge. Triamcinolone acetonide (TA) treatment induced a large LH and FSH surge at 1500 h. Similar to P(4), TA did not alter hypothalamic beta-endorphin levels during the time of the LH surge; however, after the surge, TA-treated rats had a significant increase in hypothalamic beta-endorphin levels at 1800 h (Day 29) and 0800 h the next morning. Cortisol had no effect on LH levels but increased FSH levels at 0800 h on Day 30. Similar to TA, cortisol caused an elevation in hypothalamic beta-endorphin levels at 1800 h and 0800 h the next day. Finally, pituitary dynorphin A 1-13 content was not affected by any of the steroids. This study suggests that E(2) is principally responsible for reducing hypothalamic opioid content. The stimulatory effect of progesterone and TA on gonadotropin secretion appears to be due to the turning on of an excitatory signal rather than the turning off of an inhibitory opioid signal.