NOVEL ESTROGEN FEEDBACK SITES ASSOCIATED WITH STRESS-INDUCED SUPPRESSION OF LUTEINIZING NORMONE SECRETION IN FEMALE RATS

1. The fasting-induced suppression of LH secretion is totally dependen t on steroidal milieu because the suppression is observed only in inta ct or ovariectomized estrogen-primed rats but not in ovariectomized an imals. The following neural pathway mediating fasting-induced suppress ion of LH secretion has been suggested by a series of experiment: A ne ural signal emanating from the stomach during fasting reaches the medu lla oblongata via afferent vagal nerve so as to activate the noradrene rgic system projecting to the PVN: this results in an increased CRH re lease, and in turn the suppression of the LHRH release and then LH rel ease. Estrogen seems to activate the neural pathway by acting on somew here in the pathway. 2. We found that the paraventricular nucleus of t he hypothalamus (PVN) and A2 region of the medulla oblongata is the es trogen feedback sites associated the dependence of the fasting-induced suppression of LH secretion on estrogen, The estrogen feedback action on the PVN does not involve an increase in norepinephrine release in the PVN. In addition, we also found that estrogen receptors are increa sed in the PVN and A2 region by acute fasting. Therefore, the followin g hypothesis is proposed: fasting first induces an transient increase in the activity of noradrenergic system at the beginning of the first dark phase after the food deprivation; this activation results in an i ncrease in estrogen receptors in the PVN and A2 region; the increase i n estrogen receptors leads to an increase in the sensitivity of noradr energic systems to the neural inputs associated with fasting to these nuclei. 3. The response of the reproductive activity to various extern al stimuli including stress is modulated by ovarian steroids. The estr ogen feedback action on the PVN and A2 is totally different from the s o-called ''negative feedback action'' of estrogen that is for monitori ng the ovarian condition. The novel estrogen feedback action may alter the response of neurons regulating gonadal axis to the signal associa ted with environmental cues such as stress.