Pubertal changes in pro-opiomelanocortin and gonadotropin-releasing hormone gene expression in the brain of the male monkey.

Puberty in the primate is initiated by an amplification of the pulsatile secretion of gonadotropin-releasing hormone (GnRH); however, the factors responsible for this a pubertal activation of GnRH neurons are unknown. We examined whether the biosynthetic capacity of GnRH neurons could be limiting for GnRH secretion in the juvenile monkey by determining whether the prepubertal macaque (Maraca fascicularis) expresses the GnRH gene. Using in situ hybridization for GnRH mRNA, we found no evidence for differences between prepubertal and adult animals in either the cellular level of GnRH mRNAs or the number of GnRH mRNA-containing cells in any area of the brain. These observations suggest that expression of the GnRH gene, at least to the point of messenger mRNA production, is not limiting for puberty onset. beta-Endorphin, derived from its precursor proopiomelanocortin (POMC), has been implicated as an inhibitory neurotransmitter in the control of GnRH secretion. We examined whether expression of the POMC gene changes as a function of sexual maturation by comparing the cellular content of POMC mRNA in the arcuate nucleus between prepubertal and adult male macaques. We report that cellular POMC mRNA levels are significantly higher in the adult than in the juvenile macaque (P < 0.02). We suggest that an increase in POMC biosynthesis may be part of the mechanism whereby a continuous mode of GnRH secretion is shaped into discrete pulses, which in turn initiate puberty in the primate.