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GnIH

[gonadotropin-inhibitory hormone] GnIH (SIKPSAYLPLRF-NH2) is a hypothalamic dodecapeptide hormone that inhibits gonadotropin release. It has been identified first in quail (Tsutsui et al, 2000; Satake H et al, 2001). The peptide belongs to a larger class of the so-called RFamide-related peptide (RFRP) familiy characterized by the presence of arg-phe-NH2 at the C terminus (Fukusumi et al, 2006). GnIH homologs have been identified in other vertebrates from fish to humans (Tsutsui K and Ukena K, 2006; Ukena and Tsutsui, 2005; Zhang Y et al, 2010). All peptides have a characteristic LPXRFamide (X=L or Q) motif at the C-terminus. Ubuka et al (2009) have identified human RFRP-1 [RFamide-related peptide-1] (MPHSFANLPLRF-NH2) and RFRP-3 [RFamide-related peptide-3] (VPNLPQRF-NH2) as GnIH homologs.

GnIH is encoded by the RFRP gene [abbr. for RF-amide-related peptides], which is being referred to also as NPVF [neuropeptide VF] gene (Liu et al, 2001; Schulz et al, 2002). An alternative designation is C7orf9 [[chromosome 7 open reading frame 9] (Schulz et al, 2002). The protein product of this gene is cleaved into Neuropeptide NPSF (an alternative name for Neuropeptide RFRP-1), Neuropeptide RFRP-2, and Neuropeptide NPVF (alternative designation Neuropeptide RFRP-3) (Schulz et al, 2002).

The G-protein coupled receptor, GPR147 has been identified as the cognate receptor for RFRPs in studies investigating the role of these peptides in the central nervous system (Hinuma et al, 2000). Ubuka et al (2009) have identified human GPR147 as the receptor for RFRP-1 and RFRP-3.

GnIH and its homologs appear to act as key neurohormones controlling vertebrate reproduction (Tsutsui et al, 2010; Smith JT and Clarke IJ, 2010). GnIH acts on the pituitary and neurons in the hypothalamus expressing GnRH [gonadotropin-releasing hormone]. GnIH has a direct suppressive action on the excitability of GnRH neurons (Ducret et al, 2009). GnIH inhibits basal forebrain gonadotropin-releasing hormone neurons via a direct postsynaptic mechanism (Wu et al, 2009).

Ubuka et al (2006) have reported that continuous administration of GnIH to mature quail birds decreases the expressions of gonadotropin common alpha and LH-beta subunit mRNAs as well as plasma LH and testosterone concentrations. Administration of GnIH to mature birds also induces testicular cell death by apoptosis and decreases spermatogenic activity in the testis. Singh et al (2011) have shown that GnIH inhibits follicular development and steroidogenesis in the ovary of mice. GnIH inhibits gonadal development and maintenance by decreasing gonadotropin release and synthesis. Mammalian GnIH homologs also inhibit reproduction by decreasing gonadotropin release (Pineda et al, 2010). Kirby et al (2009) have reported that GnIH affects the hypothalamic-pituitary-gonadal axis and the hypothalamic-pituitary-adrenocortical axis as stress-induced increases in adrenal glucocorticoids cause an increase in RFRP that contributes to hypothalamic suppression of reproductive function.

Neural functions of GnIH are controlled by the pineal hormone melatonin (Ubuka T et al, 2005; Chowdhury VS et al, 2010). GnIH inhibits pulsatile gonadotropin release in vivo as well as from cultured pituitary cells in sheep (Clarke et al, 2008; Sari et al, 2009) and cattle (Kadokawa et al, 2009). Quail and rat GnIH inhibit luteinizing hormone secretion in Syrian hamsters (Kriegsfeld et al, 2006) and rats (Johnson et al, 2007; Murakami et al, 2008) in vivo.


Copyright 2012 by H IBELGAUFTS. All rights reserved.
ENTRY LAST MODIFIED: October 2010



 

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