Meeting Abstract
59.1 Wednesday, Jan. 6 Cortisol masculinizes female mosquitofish morphology and behavior KNAPP, R.*; MARSH-MATTHEWS, E.C.; VO, L.; Univ. of Oklahoma, Norman; Univ. of Oklahoma, Norman; Univ. of Oklahoma, Norman rknapp@ou.edu
The ability of sex steroids to influence vertebrate sexual development and differentiation is well known. In many taxa, females can be masculinized by exposure to various androgenic compounds, some of which are human-produced. The effects of environmental androgens and estrogens on sexual development, differentiation and reproduction have been the focus of substantial study in recent years. Much less attention has been paid to effects of endocrine disrupting compounds on the glucocorticoid stress axis. We report here the unexpected finding that exposure of adult female mosquitofish (Gambusia affinis) to the stress hormone cortisol induced morphological and behavioral masculinization. Sexually-mature females were housed individually and received one of five cortisol doses or ethanol or water as controls once every three days for approximately two months. Cortisol masculinized the sexually dimorphic anal fin in a dose-dependent manner; control females were not masculinized. Masculinization of this fin is known to be under androgenic control. We also found that some cortisol-treated females attempted copulations with stimulus females with behaviors similar to those exhibited by normal G. affinis males. Males also responded differentially to cortisol-treated vs. control females, and some masculinized females attempted copulations with males. We discuss two potential mechanisms by which cortisol treatment masculinizes behavior and morphology in this species. Our results also highlight that the potential of compounds to affect the glucocorticoid axis should be considered when studying mechanisms underlying the effects of endocrine disruptors, both those that have been presumed to work only via androgenic or estrogenic pathways, as well as disruptors which are already known to affect glucocorticoid pathways.
