Abstract

Abnormal embryo cortisol level causes developmental defects and poor survival in zebrafish (Danio rerio). However, no study has demonstrated that maternal stress leads to higher embryo cortisol content in zebrafish. We tested the hypothesis that maternal stress-associated elevation in cortisol levels increases embryo cortisol content in this asynchronous breeder. Zebrafish mothers were fed cortisol-spiked food for 5 days, to mimic maternal stress, followed by daily breeding for 10 days to monitor temporal embryo cortisol content. Cortisol treatment increased mean embryo yield, but the daily fecundity was variable among the groups. Embryo cortisol content was variable in both groups over a 10-day period. A transient elevation in cortisol levels was observed in the embryos from cortisol-fed mothers only on day 3, but not on subsequent days. We tested whether excess cortisol stimulates 11βHSD2 expression in ovarian follicles as a means to regulate embryo cortisol deposition. Cortisol treatment in vitro increased 11β HSD2 levels sevenfold, and this expression was regulated by actinomycin D and cycloheximide suggesting tight regulation of cortisol levels in the ovarian follicles. We hypothesize that cortisol-induced upregulation of 11βHSD2 activity in the ovarian follicles is a mechanism restricting excess cortisol incorporation into the eggs during maternal stress.

Highlights

  • Plasma cortisol, the primary corticosteroid in teleosts, levels increase in response to stressor exposure in fishes [1]

  • Our results suggest that cortisol-mediated transcriptional upregulation of 11βHSD2 in ovarian follicles may be a key mechanism protecting embryos from elevated cortisol levels associated with maternal stress

  • We propose this tight control of embryo cortisol levels, despite the stress-induced elevation of this hormone in the mothers, as a key adaptive strategy to protect the embryo from the harmful effects of cortisol excess [4]

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Summary

Introduction

The primary corticosteroid in teleosts, levels increase in response to stressor exposure in fishes [1]. This involves the activation of hypothalamus–pituitary–interrenal (HPI) axis, including the release of corticotropin releasing factor from the hypothalamus, which stimulates the anterior pituitary to secrete adrenocorticotropic hormone (ACTH) [2,3]. ACTH acts on the interrenal tissue (analogous to the adrenal gland in mammals) to release cortisol into the circulation. Cortisol acts on target tissues to bring about physiological.

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