Abstract
While stress is known to impact reproductive performance, the pathways involved are not entirely understood. Corticosteroid effects on the functioning of the hypothalamus-pituitary-gonadal axis are thought to be a key aspect of stress-mediated reproductive dysfunction. A vital component of the stress response is the pituitary secretion of adrenocorticotropic hormone (ACTH), which binds to the melanocortin 2 receptor (MC2R) in the adrenal glands and activates cortisol biosynthesis. We recently reported MC2R mRNA abundance in fish gonads leading to the hypothesis that ACTH may be directly involved in gonadal steroid modulation. Using zebrafish (Danio rerio) ovarian follicles, we tested the hypothesis that acute ACTH stimulation modulates cortisol and estradiol (E2) secretion. ACTH neither affected cortisol nor unstimulated E2 release from ovarian follicles. However, ACTH suppressed human chorionic gonadotropin (hCG)-stimulated E2 secretion in a dose-related manner, with a maximum decrease of 62% observed at 1 I.U. ACTH mL−1. This effect of ACTH on E2 release was not observed in the presence of either 8-bromo-cAMP or forskolin, suggesting that the mechanism(s) involved in steroid attenuation was upstream of adenylyl cyclase activation. Overall, our results suggest that a stress-induced rise in plasma ACTH levels may initiate a rapid down-regulation of acute stimulated E2 biosynthesis in the zebrafish ovary, underscoring a novel physiological role for this pituitary peptide in modulating reproductive activity.
Highlights
It is well established that stress has a negative impact on reproductive processes in animals
Cortisol was not detected in media from control and adrenocorticotropic hormone (ACTH)-treated ovarian follicles after 3 h or 8 h of incubation (Fig. 2)
Cortisol was detected in follicles treated with human chorionic gonadotropin, the levels were only significantly different from the control at 3 h of incubation (Fig. 2)
Summary
It is well established that stress has a negative impact on reproductive processes in animals. The mechanisms are far from clear, the effects of stress are thought to be due to interactions of the hypothalamic-pituitary-adrenal (HPA) axis with the HP-gonadal (HPG) axis. Corticotropin releasing factor (CRF), a key hypothalamic neurohormone that activates the HPA signaling cascade, suppresses the release of hypothalamic gonadotropin-releasing hormone (GnRH) [1]. While corticosteroid is essential in order for animals to recover from exposure to a stressor, this steroid impacts the HPG axis at a number of sites, depending on the species, sex, and the magnitude and duration of this plasma hormonal response [2,3]. Cortisol inhibits GnRH pulsatility [4], and decreases gonadotropin release [follicle stimulating hormone (FSH) and luteinizing hormone (LH)] [5,6] from the pituitary. Cortisol suppresses testosterone production (reviewed by Hu et al [7]) by reducing LH responsiveness, including downregulation of LH receptors [5]
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