Abstract
While stress activates the hypothalamic–pituitary–adrenal (HPA) axis, it suppresses the hypothalamic–pituitary–gonadal (HPG) axis. Corticotropin-releasing factor (CRF) is a major regulatory peptide in the HPA axis during stress. Urocortin 1 (Ucn1), a member of the CRF family of peptides, has a variety of physiological functions and both CRF and Ucn1 contribute to the stress response via G protein-coupled seven transmembrane receptors. Ucn2 and Ucn3, which belong to a separate paralogous lineage from CRF, are highly selective for the CRF type 2 receptor (CRF2 receptor). The HPA and HPG axes interact with each other, and gonadal function and reproduction are suppressed in response to various stressors. In this review, we focus on the regulation of gonadotropins by CRF and Ucn2 in pituitary gonadotrophs and of gonadotropin-releasing hormone (GnRH) via CRF receptors in the hypothalamus. In corticotrophs, stress-induced increases in CRF stimulate Ucn2 production, which leads to the inhibition of gonadotropin secretion via the CRF2 receptor in the pituitary. GnRH in the hypothalamus is regulated by a variety of stress conditions. CRF is also involved in the suppression of the HPG axis, especially the GnRH pulse generator, via CRF receptors in the hypothalamus. Thus, complicated regulation of GnRH in the hypothalamus and gonadotropins in the pituitary via CRF receptors contributes to stress responses and adaptation of gonadal functions.
Highlights
A variety of stressors have been shown to suppress gonadal function (Chand and Lovejoy, 2011)
We focus on the regulation of gonadotropins by corticotropin-releasing factor (CRF) and Ucn2 in pituitary gonadotrophs and of gonadotropin-releasing hormone (GnRH) via CRF receptors in the hypothalamus
Proteins that play key roles in vertebrate reproduction include the neuropeptides gonadotropinreleasing hormone (GnRH) and kisspeptin and their receptors (Kim et al, 2012): kisspeptin stimulates GnRH release from hypothalamic GnRH neurons via Gpr54, a G protein-coupled receptor (Messager et al, 2005), while the gonadal steroid estrogen mediates its inhibitory effect on GnRH secretion by acting on kisspeptin-expressing neurons of the arcuate nucleus (Oakley et al, 2009; Ohkura et al, 2009)
Summary
Urocortin 1 (Ucn1), a member of the CRF family of peptides, has a variety of physiological functions and both CRF and Ucn contribute to the stress response via G protein-coupled seven transmembrane receptors. The HPA and HPG axes interact with each other, and gonadal function and reproduction are suppressed in response to various stressors. We focus on the regulation of gonadotropins by CRF and Ucn in pituitary gonadotrophs and of gonadotropin-releasing hormone (GnRH) via CRF receptors in the hypothalamus. CRF is involved in the suppression of the HPG axis, especially the GnRH pulse generator, via CRF receptors in the hypothalamus. Complicated regulation of GnRH in the hypothalamus and gonadotropins in the pituitary via CRF receptors contributes to stress responses and adaptation of gonadal functions
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