A pinboard by
Sheila Hadinia

An article by G. Y. Bédécarrats, H. McFarlane, S. R. Maddineni, R. Ramachandran


Gonadotropin inhibitory hormone may act to influence ovarian follicular maturation

In birds, as in other vertebrates, reproduction is controlled by the hypothalamo–pituitary–gonadal axis with each component secreting specific neuropeptides or hormones. Until recently, it was believed this axis is exclusively under the stimulatory control of hypothalamic gonadotropin-releasing hormone I (GnRH-I) which in turn, stimulates luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion from the pituitary gland. However, the discovery of a novel inhibitory hypothalamic peptide able to reduce LH secretion (gonadotropin-inhibitory hormone: GnIH) challenged this dogma. Furthermore, with the characterization of its specific receptor (GnIHR), progress has been made to clarify the physiological relevance of GnIH in birds.

GnIHR is a member of the G-protein coupled receptor (GPCR) family which inhibits adenylyl cyclase (AC) activity, thus reducing intracellular cAMP levels. In the chicken pituitary gland, the GnRHR-II/GnIHR ratio changes during sexual maturation in favor of GnRHR-II that appears to result in hypothalamic control of gonadotropin secretion shifting from inhibitory to stimulatory, with corresponding changes in GnRH-induced cAMP levels. Within the gonads, GnIH and its receptor may act in an autocrine/paracrine manner and may interfere with LH and FSH signaling to influence ovarian follicular maturation and recruitment, as well as spermatogenesis.