Complete medial basal hypothalamic (MBH) disconnection was performed in four immature female rhesus monkeys to determine its effects on the maturation of the mechanisms that regulate gonadotropin secretion. The sexual development of these animals, as well as that of nine control monkeys of similar bone ages, was assessed by monitoring the stimulatory feedback actions of exogenous and endogenous estrogens on LH and FSH secretion. All neuronal inputs to the hypothalamus were transsected with a Halasz-type knife resulting in “islands”of MBHH tissue comprising portions of the arcuate, ventromedial, suprachiasmatic, dorsomedial, paraventricular, and anterior and posterior hypothalamic nuclei. The disconnections produced deficits in neurohypophysial, adrenal, and thyroid secretory function, necessitating replacement with antidiuretic hormone, thyroxine, and cortisone. The postoperative administration of estradiol benzoate (42 μg/kg sc in oil) initially suppressed serum LH and FSH levels. During the 6th–8th postoperative month, however, these estrogen injections began to elicit gonadotropin discharges. Within the next 6 months, spontaneous ovulatory menstrual cycles were noted in three of the monkeys subjected to the disconnection surgery. A similar developmental pattern of the stimulatory action of estrogen was observed as the control animals matured. Furthermore, the range of bone ages at which ovulatory menstrual cycles were first observed was comparable for the control and MBH disconnected groups. It would thus appear that, in the rhesus monkey, interruption of neuronal inputs to the MBH at a bone age of approximately 2 yr does not influence the subsequent maturation of the hypothalamo-hypophysial system that regulates reproductive development and function.
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