title: Gonadotropin-releasing hormone neuronal migration.
abstract: Neurons that synthesize and secrete the decapeptide gonadotropin-releasing hormone-1 (GnRH-1) to control the reproductive axis originate in the olfactory placode/vomeronasal organ of the olfactory system of mammals and migrate along vomeronasal nerves to the cribriform plate, which marks the boundary between the peripheral olfactory system and the forebrain. Migrating GnRH-1 neurons follow a branch of the vomeronasal nerve caudally into the hypothalamus, where they extend processes to the median eminence and halt their migration. The release of GnRH-1 into the capillaries of the median eminence starts the cascade that activates pituitary gonadotropin (luteinizing hormone and follicle-stimulating hormone) production and secretion. Failure of these neurons to complete their migration results in failure of the reproductive axis. In some cases, failed migration is linked to the loss of the sense of smell (anosmia). The mechanisms that regulate migration of GnRH-1 neurons along this complex pathway are incompletely understood. Recent studies have revealed an important role for a series of strategically located soluble factors that regulate different aspects of GnRH-1 neuron migration at specific locations along their migratory route. This review focuses on the different mechanisms used by these factors to regulate migration of GnRH-1 neurons.
authors: Shriver Center and Department of Cell Biology, University of Massachusetts Medical School, Waltham, MA, USA.
authors: Gerald A
authors: GA
authors: Schwarting
authors: Margaret E
authors: ME
authors: Wierman
authors: Stuart A
authors: SA
authors: Tobet
mesh_terms: D000818:Animals; D002465:Cell Movement; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D006801:Humans; D007006:Hypogonadism / Q000378:metabolism / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000254:growth & development / Q000378:metabolism*; D017436:Kallmann Syndrome / Q000378:metabolism / Q000503:physiopathology; D059648:Kisspeptins; D009414:Nerve Growth Factors / Q000378:metabolism; D000075388:Netrin-1; D009474:Neurons / Q000378:metabolism*; D009833:Olfactory Pathways / Q000254:growth & development / Q000378:metabolism; D016548:Prosencephalon / Q000254:growth & development / Q000378:metabolism; D011498:Protein Precursors / Q000378:metabolism*; D019718:Receptors, CXCR4 / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D000074502:Receptors, Kisspeptin-1; D012098:Reproduction; D015398:Signal Transduction; D025521:Tumor Suppressor Proteins / Q000378:metabolism
chemical_list: C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; C106628:KISS1 protein, human; C118688:KISS1R protein, human; D059648:Kisspeptins; D009414:Nerve Growth Factors; D011498:Protein Precursors; D019718:Receptors, CXCR4; D043562:Receptors, G-Protein-Coupled; D000074502:Receptors, Kisspeptin-1; D025521:Tumor Suppressor Proteins; C050866:progonadoliberin I; D000075388:Netrin-1; D007987:Gonadotropin-Releasing Hormone