While previous studies have demonstrated the presence of estrogenic compounds in waste water effluent, there is limited knowledge of how these compounds impact the regulatory pathways of the brain in mature fish. These studies illustrated that fish exposed to exogenous estrogens exhibit decreased proliferation of the brain and elevated expression of aromatase B (cyp19a1b) and estrogen receptor 2b (esr2b). In this study, male zebrafish (n=12) were exposed to exogenous ethinylestradiol (EE2), at environmentally relevant concentrations (0, 2.5, and 25 ng/L), for seven-days, to examine its effect on the regulatory pathways which controls neural progenitors proliferation in the hypothalamus and telencephalon. The liver of each fish was examined for changes in the expression of vitellogenin (vtg), to confirm that the EE2 was taken up by the fish at levels that would upregulate vtg expression. Changes in the estrogen regulated proliferation pathway were monitored via the expression of esr2b, cy19a1b, and proliferating cellular nuclear antigen (pcna) (n=8). Although liver vtg expression was significantly upregulated when exposed to the high treatment, no differences in the expression of cy19a1b, esr2b, or pcna in the brain were detected. The lack of change in proliferation, noted by differences in the expression of pcna between treatments is predicted to be due to EE2 not effecting the expression of cy19a1b and esr2b, which control early steps of the regulatory pathway. Estrogen regulated pathways are an important part of the physiology of brains and should be examined further in case higher concentrations can induce proliferation of the brain by impacting cyp19a1b and esr2b expression.