TY - JOUR
T1 - Progesterone and corticosteroid regulation of hypothalamic and pituitary opioid content during LH surge induction
AU - Brann, Darrell W.
AU - Putnam-Roberts, Carla D.
AU - Mahesh, Virendra B.
PY - 1992/6
Y1 - 1992/6
N2 - 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 (E2) (2 μg) for 2 days. E2 treatment markedly suppressed hypothalamic β-endorphin content at 1500 h, 1800 h (Day 29), and 0800 h (Day 30) but had no effect on pituitary β-endorphin levels. The administration of progesterone (P4) 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 β-endorphin content was unchanged during the LH surge induced by P4, although a nonsignificant elevation of hypothalamic β-endorphin levels was noticed in P4-treated rats the morning after the surge. Triamcinolone acetonide (TA) treatment induced a large LH and FSH surge at 1500 h. Similar to P4, TA did not alter hypothalamic β-endorphin levels during the time of the LH surge; however, after the surge, TA-treated rats had a significant increase in hypothalamic β-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 β-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 E2 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.
AB - 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 (E2) (2 μg) for 2 days. E2 treatment markedly suppressed hypothalamic β-endorphin content at 1500 h, 1800 h (Day 29), and 0800 h (Day 30) but had no effect on pituitary β-endorphin levels. The administration of progesterone (P4) 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 β-endorphin content was unchanged during the LH surge induced by P4, although a nonsignificant elevation of hypothalamic β-endorphin levels was noticed in P4-treated rats the morning after the surge. Triamcinolone acetonide (TA) treatment induced a large LH and FSH surge at 1500 h. Similar to P4, TA did not alter hypothalamic β-endorphin levels during the time of the LH surge; however, after the surge, TA-treated rats had a significant increase in hypothalamic β-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 β-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 E2 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.
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U2 - 10.1016/1044-7431(92)90038-4
DO - 10.1016/1044-7431(92)90038-4
M3 - Article
AN - SCOPUS:0026747646
SN - 1044-7431
VL - 3
SP - 191
EP - 198
JO - Molecular and Cellular Neuroscience
JF - Molecular and Cellular Neuroscience
IS - 3
ER -