Endocrine Abstracts

The initiation of mammalian puberty requires an increased pulsatile release of gonadotrophin hormone releasing hormone (GnRH) from the hypothalamus. This increase is brought about by changes in transsynaptic and glial–neuronal communication. Coordination of this regulatory neuronal–glial network likely requires the participation of a multiplicity of genes hierarchically arranged within discrete, but interactive, networks. The identity and structural features of at le...

GnRH agonists continually stimulate the pituitary gonadotrophs, leading to desensitization and decreases in LH release and, to a lesser extent, FSH release after an initial flare-up. They have transformed the management of precocious puberty since their initial use in early 80’s. However, several issues remain unresolved that are pertinent to the indications and use of these medications. Different GnRH agonists are available in various depot forms and their use results in...

The recent discovery of the importance of kisspeptin-GPR54 signaling to the onset of puberty in humans has generated intense interest in understanding the mechanisms and pathways of kisspeptin-GPR54 signaling at the gonadotropin-releasing hormone (GnRH) neurons. Using transgenic mouse models, electrophysiology and immunocytochemistry we have shown that kisspeptin strongly activates adult GnRH neurons and that these cells receive a direct input from kisspeptin neurons located i...

Pubertal onset results from reactivation of the gonadotropic axis by neuroendocrine mechanisms which remain to be defined. Human genetics is one of the approaches to characterize disease mechanisms and therefore novel physiological system. Two different type of phenotype due to abnormal timing of the pubertal onset are described: advance of the pubertal onset also call central precocious puberty and delayed or absence of puberty. The latter is due to gonadotropic deficiency re...