1-(o-Chlorophenyl)-1 (p-chlorophenyl)2,2,2-trichloroethane induces functional progestin receptors in the rat hypothalamus and pituitary gland.

A recent report suggests that estrogen induction of hypothalamic progestin receptors is not a prerequisite for the facilitation by progesterone of female sexual behavior in rats. Progesterone was found to facilitate sexual behavior despite no apparent induction of progestin receptors by 1-(o-chlorophenyl) 1-(p-chlorophenyl)2,2,2-trichloroethane (o,p'-DDT). To investigate these findings further, ovariectomized rats were treated with daily injections of o,p'-DDT for 3 days, followed by progesterone on day 4. Daily injections of 400 mg o,p'-DDT/kg resulted in activation of lordosis in 50% of the animals; injections of 200 mg/kg were ineffective. Cytoplasmic and nuclear progestin receptor levels in the mediobasal hypothalamus-preoptic area and pituitary gland were then determined in similarly treated animals. Because competition assays revealed that o,p'DDT interacts with progestin-binding sites in vitro, residual o,p'-DDT was removed from the cytosol fraction before assay. o,p'-DDT treatment increased the level of cytoplasmic progestin receptors by 43% compared with that in oil-injected controls. Progesterone administration to DDT-treated rats resulted in a 137% increase in the level of nuclear progestin receptors relative to levels observed in animals receiving no progesterone. These findings contradict a previous report using o,p'-DDT and support the hypothesis that estrogen-induced progestin receptors are required for the facilitation of sexual receptivity by progesterone.