Gestational Sympathetic Stress Programs the Fertility of Offspring: A Rat Multi-Generation Study.

Beatriz Piquer,Freddy Ruz,Hernan E. Lara,Rafael Barra

doi:10.3390/ijerph19053044

Abstract

The exposure to sympathetic stress during the entire period of gestation (4 °C/3 h/day) strongly affects the postnatal reproductive performance of the first generation of female offspring and their fertility capacity. The aim of this work was to determine whether this exposure to sympathetic stress affects the reproductive capacity of the next three generations of female offspring as adults. Adult female Sprague–Dawley rats were mated with males of proven fertility. We studied the reproductive capacity of the second, third, and fourth generations of female offspring (the percentage of pregnancy and the number and weight of female offspring). The estrus cycle activity of the progenies was studied, and a morphological analysis of the ovaries was carried out to study the follicular population. The second generation had a lower number of pups per litter and a 20% decrease in fertile capacity. The estrus cycle activity of the third generation decreased even more, and they had a 50% decrease in their fertile capacity, and their ovaries presented polycystic morphology. The fourth generation however, recovered their reproductive capacity but not the amount of newborns pups. Most probably, the chronic intrauterine exposure to the sympathetic stress programs the female gonads to be stressed in a stressful environment; since the fourth generation was the first born with no direct exposure to stress during development, it opens studies on intrauterine factors affecting early follicular development.

Highlights

All living organisms are moldable in their first moments of life and during pregnancy, so they adapt to the conditions they find in the placental environment
If chronic stress occurs during the gestation period, this stress is capable of modifying the placental environment and producing lasting changes in the embryos, which may affect the development of organs, the physiology, and the metabolism of the organism, something known as fetal programming [4,5]
Stress can activate various pathways: the hypothalamic–pituitary–adrenal (HPA) axis, which produces the release of adrenocorticotropic hormone (ACTH) and adrenaline (A), and/or the activation of the sympathetic nervous system (SNS), which produces the release of noradrenaline (NE)

Summary

Introduction

All living organisms are moldable in their first moments of life and during pregnancy, so they adapt to the conditions they find in the placental environment. This flexibility allows them to adapt to the surrounding environment without being influenced exclusively by their genetic load, which is much faster than genetic adaptation [1–3]. Stress is defined as any stimulus capable of altering the organism’s homeostasis; it is necessary for survival and is the organism’s way of dealing with a threatening situation. Stress can activate various pathways: the hypothalamic–pituitary–adrenal (HPA) axis, which produces the release of adrenocorticotropic hormone (ACTH) and adrenaline (A), and/or the activation of the sympathetic nervous system (SNS), which produces the release of noradrenaline (NE). The activation of the SNS is observed in “fight or flight” situations, as would be in the case of a cold situation without hypothermia [1,6,7]

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