title: Gonadotropin-inhibitory hormone inhibits gonadal development and maintenance by decreasing gonadotropin synthesis and release in male quail.
abstract: Until recently, any neuropeptide that directly inhibits gonadotropin secretion had not been identified. We recently identified a novel hypothalamic dodecapeptide that directly inhibits gonadotropin release in quail and termed it gonadotropin-inhibitory hormone (GnIH). The action of GnIH on the inhibition of gonadotropin release is mediated by a novel G protein-coupled receptor in the quail pituitary. This new gonadotropin inhibitory system is considered to be a widespread property of birds and provides us with an unprecedented opportunity to study the regulation of avian reproduction from an entirely novel standpoint. To understand the physiological role(s) of GnIH in avian reproduction, we investigated GnIH actions on gonadal development and maintenance in male quail. Continuous administration of GnIH to mature birds via osmotic pumps for 2 wk decreased the expressions of gonadotropin common alpha and LHbeta subunit mRNAs in a dose-dependent manner. Plasma LH and testosterone concentrations were also decreased dose dependently. Furthermore, administration of GnIH to mature birds induced testicular apoptosis and decreased spermatogenic activity in the testis. In immature birds, daily administration of GnIH for 2 wk suppressed normal testicular growth and rise in plasma testosterone concentrations. An inhibition of juvenile molt also occurred after GnIH administration. These results indicate that GnIH inhibits gonadal development and maintenance through the decrease in gonadotropin synthesis and release. GnIH may explain the phenomenon of photoperiod-induced gonadal regression before an observable decline in hypothalamic GnRH in quail. To our knowledge, GnIH is the first identified hypothalamic neuropeptide inhibiting reproductive function in any vertebrate class.
authors.affiliation: Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan.
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Ubuka
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Ukena
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Sharp
authors.forename: George E
authors.initials: GE
authors.lastname: Bentley
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Tsutsui
mesh_terms: D000818:Animals; D017209:Apoptosis; D030161:Avian Proteins / Q000494:pharmacology*; D001835:Body Weight; D003370:Coturnix; D017931:DNA Primers / Q000737:chemistry; D004305:Dose-Response Relationship, Drug; D037201:Follicle Stimulating Hormone, beta Subunit / Q000378:metabolism; D005786:Gene Expression Regulation; D006062:Gonadotropins / Q000378:metabolism*; D007028:Hypothalamic Hormones / Q000494:pharmacology*; D007031:Hypothalamus / Q000378:metabolism / Q000473:pathology; D020287:In Situ Nick-End Labeling; D007986:Luteinizing Hormone / Q000378:metabolism; D037101:Luteinizing Hormone, beta Subunit / Q000378:metabolism; D008297:Male; D009479:Neuropeptides / Q000737:chemistry; D010455:Peptides / Q000737:chemistry; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D011863:Radioimmunoassay; D012671:Seminiferous Tubules / Q000378:metabolism; D012708:Sertoli Cells / Q000378:metabolism; D013091:Spermatogenesis; D013737:Testis / Q000187:drug effects / Q000378:metabolism; D013739:Testosterone / Q000097:blood / Q000378:metabolism; D013997:Time Factors
chemical_list: D030161:Avian Proteins; D017931:DNA Primers; D037201:Follicle Stimulating Hormone, beta Subunit; D006062:Gonadotropins; D007028:Hypothalamic Hormones; D037101:Luteinizing Hormone, beta Subunit; D009479:Neuropeptides; D010455:Peptides; D012333:RNA, Messenger; C413752:gonadotropin-inhibitory hormone, Coturnix japonica; D013739:Testosterone; D007986:Luteinizing Hormone