Abstract
Physical and psychological stressors suppress hypothalamic–pituitary–gonadal axis activity and sexual behavior and consequently induce reproductive dysfunction. Recently, it has been shown that gonadotropin-inhibitory hormone (GnIH), also called RFamide-related peptide 3 (RFRP) in mammals, which is a potent inhibitory regulator of gonadotropin-releasing hormone (GnRH) and gonadotropin, is involved in stress-induced reproductive dysfunction. GnIH/Rfrp (the gene coding RFRP-3) expression and activity are increased by psychological and immune stress, and this alteration suppresses GnRH and gonadotropin secretion. Glucocorticoid acts as a mediator that interacts between stress and hypothalamic GnIH/RFRP-3. GnIH/RFRP-3 also plays important roles in stress-induced suppression of sexual behavior and infertility, and genetic silencing of GnIH/Rfrp completely recovers sexual behavior and fertility. This review summarizes what is currently known about the roles of GnIH in stress-induced reproductive dysfunction.
Highlights
Humans and animals have a finite amount of energy for their activities
This paper presents a review of what is currently known about the roles of gonadotropin-inhibitory hormone (GnIH)/RFamide-related peptide 3 (RFRP)-3 in stress-induced reproductive dysfunction in experimental animals
Lopes et al have shown in birds that an injection of 2 mg/kg of LPS suppressed gonadotropin-releasing hormone (GnRH) mRNA and peptide expressions 2 h after injection, but did not affect GnIH [37]. These results suggest that the underlying mechanisms of dysfunction of gonadotropin secretion are changed according to the severity of immune stress, and that changes of some reserve factors, i.e., GnIH/RFRP-3, begin to participate in the suppression of GnRH and gonadotropin under severe conditions
Summary
Humans and animals have a finite amount of energy for their activities. if any activity has to be energetically prioritized, energy for other activities will be suppressed. These stresses induce some sickness behaviors, and they suppress HPG activity through inhibition of GnRH synthesis and secretion in several mammals and birds [10,11,12,13,14,15,16,17]. This neuropeptide was named gonadotropin-inhibitory hormone (GnIH), and later studies have shown that GnIH and its receptor, G-protein-coupled receptor (GPR) 147, have pivotal roles in the regulation of physiological function of the HPG axis, such as GnRH pulses and surges, in many species [20,21,22].
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