The duration of lactational infertility is significantly lengthened in young primate mothers. We hypothesize that altered neuroendocrine regulation of ovulation in adolescents synergizes with the nursing-induced inhibition of ovarian function to greatly reduce the reproductive capacity in young females. A series of longitudinal studies will evaluate the hypotheses that (1) nursing suppresses ovarian function by suckling-induced decreases in gonadotropin-releasing hormone (GnRH) secretion, and thus luteinizing hormone (LH) and follicle stimulating hormone (FSH) and (2) sexually mature adolescent females are more responsive to estradiol (E2) negative feedback and nongonadal restraint of LH and FSH release. The use of seasonal breeding rhesus monkeys will identify the biobehavioral factors which maintain lactational infertility at a time which is optimal-fbr the occurrence of ovulations in nonlactating females. We will determine how quantifiable changes in nursing behavior alter the neuroendocrine control of ovarian function. The resilience of episodic LH and FSH release and pituitary sensitivity to GnRH will be assessed in adult and adolescent mothers following removal of the suckling stimulus during mid and late lactation. Pulsatile infusion of one of three doses of GnRH to reinitiate ovulatory cycles will evaluate the hypothesis that lactation disrupts endogenous GnRH secretion and will determine if adolescent mothers are less responsive to this treatment. These studies will also assess the direct effects of nursing on ovarian function in the presence of appropriate LH and FSH support. Further dose-response studies will determine if suckling and adolescent status affect LH and FSH secretion by enhanced E2 negative feedback or the induction of nongonadal restraint. An examination of periparturitional levels of prolactin (PRL) will determine if these are predictive of eventual neuroendocrine deficits in adolescent mothers. Also, studies will elucidate how lactation and adolescence diminish ovulatory capacity during the breeding season by assessing the effects of low intensity nursing on episodic LH and FSH release and subsequent ovarian responsiveness. Finally, the behavioral and physiological antecedents which initiate changes in nursing behavior will be described. The manipulation of both nursing behavior and serum PRL levels will determine the differential contribution of each variable to the maintenance of lactation infertility. These studies will describe the basic mechanisms which regulate lac- tational infertility in primates and how it is prolonged in adolescent mothers.
