Abstract

The reproduction of seasonal breeders is modulated by exposure to light in an interval of 24 h defined as photoperiod. The interruption of reproductive functions in seasonally breeding rodents is accompanied by the suppression of the Kiss1 gene expression, which is known to be essential for reproduction. In non-seasonal male rodents, such as rats and mice, short-day photoperiod (SP) conditions or exogenous melatonin treatment also have anti-gonadotropic effects; however, whether photoperiod is able to modulate the puberty onset or Kiss1 gene expression in mice is unknown. In the present study, we investigated whether photoperiodism influences the sexual maturation of female mice via changes in the kisspeptin system. We observed that SP condition delayed the timing of puberty in female mice, decreased the hypothalamic expression of genes related to the reproductive axis and reduced the number of Kiss1-expressing neurons in the rostral hypothalamus. However, SP also reduced the body weight gain during development and affected the expression of neuropeptides involved in the energy balance regulation. When body weight was recovered via a reduction in litter size, the timing of puberty in mice born and raised in SP was advanced and the effects in hypothalamic mRNA expression were reverted. These results suggest that the SP delays the timing of puberty in female mice via changes in the kisspeptin system, although the effects on hypothalamic–pituitary–gonadal axis are likely secondary to changes in body weight gain.

Highlights

  • Photoperiod duration is one of the most potent environmental cues responsible for synchronizing daily variations in mammalian physiology, including factors that control the reproductive system

  • Because photoperiodism has been previously shown to influence the body weight of seasonally and non-seasonally breeding rodents [11, 12, 25, 26], we evaluated in more detail whether the short-day photoperiod (SP) could affect the body weight gain during development

  • Our findings showed that mice born and raised in SP exhibited a lower body weight gain throughout development (Figure 1J; P = 0.0005)

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Summary

Introduction

Photoperiod duration is one of the most potent environmental cues responsible for synchronizing daily variations in mammalian physiology, including factors that control the reproductive system. The mechanism by which the light/dark cycle synchronizes biological functions in mammals relies on the suprachiasmatic nuclei (SCN), which are considered the master clock that coordinates daily rhythms. The lack of circadian rhythms, as induced by SCN ablation, or free-running rhythms, as induced by constant light, leads to reproductive deficits as demonstrated by impairment of ovulation, disruption of the estrous cycle and LH surge [3,4,5]. SCN [6, 7], and is considered an important factor for the control of reproduction in melatonin-proficient mammals. Estrous cyclicity can be reestablished by exogenous melatonin administration in female rats exposed to constant light [5]. The neuroendocrine mechanisms by which variations in photoperiod modulate the hypothalamus–pituitary–gonadal (HPG) axis are not fully understood

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