The Consequences Of Puberty

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Puberty is considered to be a period of transition consisting of both physiological and morphological changes when an individual becomes a fecund adult from a juvenile. All mammals undergo puberty (1) although the precise timing of this event is different for each species. Pubertal onset, in mammals, is governed by the pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH promotes secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland which in turn stimulate the gonads. This process ultimately leads to the development of secondary sexual characteristics. The starting point for the hypothalamic-pituitary-gonadal (HPG) axis is GnRH and its secretion is controlled …show more content…
GnRH is released from the hypothalamus (see fig 1), passes via the portal system to the pituitary to stimulate the release of gonadotrophins from the adenohypophysis. In men LH stimulates the Leydig cells present in the testes to secrete testosterone whilst FSH binds to the Sertoli cells and promotes spermatogenesis. In women the LH leads to ovulation whilst FSH stimulates the Granulosa cells and initiates follicular growth. It is known (2) that the GnRH neurones migrate from the olfactory placode along the vomeronasal nerves. The factors that control this migration are not completely understood. One gene involved in the migration (3) of GnRH neurones is the KAL1, which encodes the protein anosmin-1. This gene is located on the x chromosome and is required for both olfactory receptor neurones and GnRH neurones to enter the brain. This gives rise to the symptoms of anosmia and hypogonadotropic hypogonadism. There are other mutations which affect GnRH neuronal migration. The fibroblast growth factor receptor 1, encoded by the FGFR1 (4) gene, is important in the development of olfactory receptors. Another example of a mutation in a gene causing failure of GnRH neuronal migration is with the NELF (5) gene that encoded for nasal embryonic LH-releasing hormone factor (NELF). NELF is needed for the attachment of GnRH neurones to the olfactory receptor axons. The GnRH neurones attach and …show more content…
The GPR54-deficient mice had hypogonadotropic hypogonadism, indicated by the small testes in the male mice and an absence of follicular maturation in the female mice. The study found that the mice had significantly lower serum concentrations of FSH and LH. But when GnRH was administered to the mice, the concentration of serum LH increased five-fold (7). This suggests that there is no problem with the pituitary or the cells that secrete the gonadotrophs but higher up in the hypothalamus. The concentration of GnRH is too low to elicit a response from the pituitary gland. Hence, the condition should be hypothalamic hypogonadism as the problem higher up than the pituitary gland. Interestingly the concentrations of GnRH in the hypothalamus of the GPR54-deficient mice were not dissimilar to normal mice. This is also considered to be true in nonhuman, prepubescent primates and rats as it has been found that they have normal mRNA concentrations of GnRH and a normal number of GnRH-containing neurones. The difference being that before puberty mammals do not secrete the levels of GnRH that are seen after and during the puberty. Kisspeptin and its receptor seem to be key in causing higher concentrations of GnRH to be secreted. It may work by modifying the processing of GnRH or by direct stimulation of the GnRH neurones to secrete. In either case, mammals without

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