Abstract
BackgroundPuberty onset is a complex, organized biological process with multilevel regulation, and its physiopathological mechanisms are yet to be elucidated. RFRP-3, the mammalian ortholog to gonadotropin-inhibitory hormone, is implicated in inhibiting the synthesis and release of gonadotropin in mammals. However, it is unclear whether RFRP-3 participates in regulating pubertal development.MethodsThis study investigated the functional significance and regulatory mechanism of hypothalamic RFRP-3 neuropeptide in the onset of puberty in young female rats. On postnatal day 22, we implanted cannulas into the lateral ventricles of female rat pups. From postnatal day 28 to postnatal day 36, the intracerebroventricular injection of RFRP-3, or vehicle, was conducted twice a day. To investigate whether puberty onset was affected, we examined the body weight, age of vaginal opening, serum hormone levels, uterus and ovary development, and hypothalamic Kiss-1 mRNA expression.ResultsIntracerebroventricular injection of RFRP-3 significantly decreased the serum concentrations of luteinizing hormone and estradiol, delayed uterine maturation, and postponed the time of vaginal opening. This study suggests that RFRP-3 can delay the onset of puberty in young female rats; the expression of Kiss-1 mRNA is potently inhibited in the RFRP-3 group. Moreover, our data show that RFRP-3 elevates serum growth hormone levels.ConclusionsThese data suggest that intracerebroventricular injection of RFRP-3 significantly delays the onset of puberty in female rats. Additionally, RFRP-3 may be associated with prepubertal rise in the secretion of growth hormone.
Highlights
Puberty onset is a complex, organized biological process with multilevel regulation, and its physiopathological mechanisms are yet to be elucidated
Our study is the first to reveal that ICV injection of RFamide-related peptide-3 (RFRP-3) of prepubertal female rats can delay the timing of puberty onset
RFRP-3 inhibited the central expression of hypothalamic Kiss-1 mRNA, suggesting that Kiss-1 may be one of the action sites in RFRP-3-delayed puberty onset
Summary
Puberty onset is a complex, organized biological process with multilevel regulation, and its physiopathological mechanisms are yet to be elucidated. RFRP-3, the mammalian ortholog to gonadotropininhibitory hormone, is implicated in inhibiting the synthesis and release of gonadotropin in mammals. It is unclear whether RFRP-3 participates in regulating pubertal development. The onset of puberty is a well-organized biological process controlled by the reproductive neuroendocrine systems [1, 2]. It is governed by high-frequency hypothalamic gonadotropin-releasing hormone (GnRH) pulsing [3,4,5,6]. Numerous studies suggest that the kisspeptin/GPR54 system is the trigger for puberty onset [18,19,20,21]
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