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Gonadal quiescence prior to puberty in primates results from a diminished secretion of the pituitary gonadotropic hormones, follicle-stimulating hormone and luteinizing hormone, which, in turn, is occasioned by an interruption of pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus during this phase of development. A discharge of GnRH may be provoked from the hypothalamus of prepubertal monkeys, however, by an i.v. injection of N-methyl-D-aspartate (NMDA), an analog of the putative excitatory neurotransmitter, aspartate. Since this action of NMDA is blocked by the specific NMDA receptor antagonist, DL-2-amino-5-phosphonopentanoic acid, the release of GnRH is likely mediated by NMDA receptors located either on the GnRH neurons themselves or on afferents to the GnRH cells. We report here that prolonged intermittent NMDA stimulation of GnRH neurons within the hypothalamus of the juvenile monkey for 16-30 wk results, with surprising ease, in the onset of precocious puberty with full activation of the hypothalamic-pituitary-Leydig cell axis and initiation of spermatogenesis. These findings demonstrate that, in primates, the network of hypothalamic GnRH neurons, which in adulthood provides the drive to the gonadotropin-secreting cells of the anterior pituitary gland, must now be viewed together with the pituitary and gonads as a nonlimiting component of the control system that governs the onset of puberty in these species.

Puberty in monkeys is triggered by chemical stimulation of the hypothalamus.