EFFECTS OF FOOD-DEPRIVATION ON INDUCTION OF NEURAL PROGESTIN RECEPTORS BY ESTRADIOL IN SYRIAN-HAMSTERS

Food deprivation, as well as treatment with metabolic inhibitors, supp ress steroid hormone-induced estrous behavior in ovariectomized (OVX) Syrian hamsters. Previous work indicates that 48 h of food deprivation decreases the number of detectable estrogen receptor immunoreactive ( ERIR) cells in the ventromedial hypothalamus (VMH) and the area just l ateral to it (VLH), increases the number of ERIR cells in the medial p reoptic area (MPO), and has no effect on the number of ERIR cells in t he nucleus of the solitary tract in OVX hamsters. The present study ex amined the effects of food deprivation on neural progestin receptor bi nding using an in vitro binding assay and on progestin receptor immuno reactivity (PRIR) in estradiol-primed, OVX hamsters. Parallel behavior tests for sexual behavior were also performed in both experiments. OV X hamsters received 2.5 mu g estradiol benzoate and were fed ad libitu m or food deprived at the same time. Forty-eight hours later, animals were killed in preparation for the immunocytochemistry or progestin re ceptor assay. Binding assays indicated that 48-h food deprivation decr eased progestin receptor levels in the preoptic area and had no effect in the mediobasal hypothalamus, an area that includes the VMH and the arcuate nucleus (ARH). Immunocytochemical analysis confirmed these fi ndings. Food deprivation caused a decrease in sexual receptivity and i n the number of detectable PRIR cells in the MPO and medial amygdala b ut had no effect on the number of detectable PRIR cells in the VMH/VLH , the ARH, or the anteroventral periventricular nucleus. These results suggest that food deprivation modulates progestin receptor binding an d PRIR in a site-specific manner. In addition, the effects of food dep rivation on neural ERIR and PRIR are significantly different.