Effects of sex steroids on brain β-endorphin

Brain β-endorphin was measured by radioimmunoassay in female rats during different stages of the estrous cycle, during pregnancy, 3 weeks after ovariectomy, and 3 weeks after ovariectomy plus estradiol or estradiol and progesterone replacement. No change in hypothalamic β-endorphin content was noted on the afternoon of diestrus, proestrus, or estrus. However, in 9 rats studied between days 8–20 of pregnancy the mean hypothalamic β-endorphin concentration of41.6 ± 2.24ng/mg protein was significantly higher than the concentration of32.7 ± 1.01 in 21 non-pregnant animals (P < 0.001). Although hypothalamic β-endorphin content did not change 3 weeks after ovariectomy, when ovariectomized rats were treated iwth silastic estradiol capsules for 3 weeks, hypothalami β-endorphin decreased significantly from25.5 ± 1.2to18.3 ± 1.3and15.5 ± 0.94ng/mg protein after low and high dose estradiol treatment respectively (P < 0.001). In a second experiment hypothalamic β-endorphin in ovariectomized rats decreased from27.1 ± 1.5to20.7 ± 1.9ng/mg protein after 3 weeks of estradiol treatment (P < 0.02); the β-endorphin content of the thalamus and midbrain also decreased from8.95 ± 1.5and4.11 ± 0.70to5.24 ± 0.39and2.42 ± 0.25ng/mg protein, respectively (P < 0.025). When progesterone was administered together with estradiol, the decrease in β-endorphin induced in the hypothalamus, thalamus and midbrain by estradiol treatment was partially blocked and β-endorphin concentrations in the latter two regions were no longer significantly different from controls. We conclude that physiologic concentrations of estradiol and progesterone can alter the content of brain β-endorphin and suggest that ovarian steroids may be important regulators of this brain peptide.