| Abstract: | It has been previously shown that treatment with estradiol valerate (EV) or 17 beta-estradiol produces enhanced tritiated naloxone binding in the hypothalamus of the rat. In the present study, the following questions were addressed: Does this effect occur in the preoptic and anterior hypothalamic areas (regions associated with the cyclic gonadotropin surge)? Is chronic estradiol (E2) exposure essential in producing a long-term elevation in opiate binding? Is the effect steroid specific? The results indicated that chronic, but not acute, exposure to estradiol induces and maintains enhanced binding in the anterior hypothalamus. E2 exposure was most effective in this regard, testosterone (T) significantly less so, and 5 alpha-dihydrotestosterone (DHT) caused no elevation in binding above castrate control levels. Furthermore, both T and DHT significantly inhibited the estradiol effect. In addition, intact animals showed significantly less binding than their ovariectomized counterparts, suggesting that the ovary normally produces a factor that suppresses opiate binding. Enhancement of anterior hypothalamic opiate binding is therefore dependent on chronic exposure to E2, and the marginal effects of T are probably due to in situ aromatization. E2 enhancement of opiate binding may be causal in producing the hypothalamic aberration that results in the EV-induced polycystic ovarian condition. |
