Meeting Abstract
Gonadotropin-inhibitory hormone (GnIH) is synthesized in the hypothalamus and gonads and can influence all levels of the reproductive axis. In the gonads, GnIH can down-regulate expression of steroidogenic enzymes, thereby reducing production of sex steroids. Corticosterone and metabolic stress can induce GnIH expression in the gonads in vitro, suggesting that GnIH may mediate stress-induced decreases in circulating sex steroids. Previously, we found that acute restraint stress increased expression of GnIH in zebra finch testes. In the present study, we hypothesized that GnIH in the ovaries would respond to acute restraint stress, but that the response would differ according to the reproductive status of the female (hierarchical vs. non-hierarchical ovarian follicles). To test this, we collected ovaries in different stages of development from females immediately after capture or following 60 minutes of restraint. Restraint significantly increased plasma corticosterone and average expression of GnIH across the ovary. The increase in GnIH expression appeared to be driven by expression in small white (SW) follicles. GnIH expression in this follicle type increased significantly with restraint stress but, within restrained females, did not differ between females with a hierarchical vs. non-hierarchical ovary. Expression of steroidogenic acute regulatory (StAR) protein did not differ significantly with restraint stress. Other steroidogenic enzymes (3BHSD, 17BHSD, aromatase) are potential targets for regulation by stress and GnIH. Further research will address whether GnIH in the SW follicles is acting in an autocrine or paracrine manner to control steroidogenesis in adjacent ovarian follicles.
