Document Type

Honors Thesis

Publication Date

5-2014

Abstract

It is traditionally understood that sex steroid hormones work through slow genomic pathways. More recently, it has also been discovered that sex steroid hormones also mediate rapid effects through a non-genomic pathway. However, much is still unknown about this mechanism, such as the receptors that mediate these effects, the behavioral consequences, and the contexts in which they occur. Goldfish have been used to investigate these behavioral effects and the receptors used in a sexual social context. To explore these ideas, the Thompson Lab and I tested if sex pheromones that rapidly increase levels of testosterone could also rapidly increase milt and/or courtship behavior, and if any such effects are blocked by the administration of fadrozole (FAD). We also used immunohistochemistry (IHC) to see if we could identify traditional estrogen receptors that might participate in non-genomic regulatory mechanisms. The results from my experiments show that milt increases in the presence of prostaglandin F2 alpha (PGF2α) and 17, 20 beta-dihydroxy-4-pregnen-3-one (17, 20 BP). FAD blocked the 17, 20 BP induced milt response in one experiment, and though it reduced the milt increases stimulated by a combined 17, 20 BP and female exposure in a subsequent experiment, the effect was not significant. In fact, FAD significantly increased milt in the absence of any other social stimuli. This response of increased milt may suggest rapid androgenic effects on these responses. Our IHC experiments demonstrated non-nuclear localization of two estrogen receptors, ERß and GPR 30, suggesting one or both may mediate estradiol’s rapid effects on physiology and behavior in goldfish.

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