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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: J Neuroendocrinol. 2016 Jul;28(7):10.1111/jne.12401. doi: 10.1111/jne.12401

Figure 1.

Figure 1

Response of male fetal hypothalamic-pituitary-testis axis to vehicle (Control), androgen antagonist flutamide and androgen agonist dihydrotestosterone (DHT). Pregnant ewes received injections of vehicle, flutamide and DHT from gestation day (GD) 60 to 84 and fetuses were delivered on GD85 for evaluation. In control eugonadal male fetuses, LH secretion is tonically suppressed by androgens at this age to regulate normal testosterone (T) secretion driving normal androgen action which, in turn, masculinizes the ovine sexually dimorphic nucleus (oSDN). Exposure to flutamide blocks negative feedback resulting in elevated LH concentrations, enlarged testis & increased testicular T secretion. The increased T competes with the competitive antagonist flutamide for the androgen receptor and leads to partial, instead of full, inhibition of oSDN masculinization. Exogenous DHT exposure enhances negative feedback further suppressing LH secretion leading to smaller testis and reduced levels of testicular T. The result of DHT treatment is reduced exposure of the developing SDN to endogenous T and incomplete masculinization. Both results are consistent with a role for androgen receptor activation in the masculinization of the ovine SDN.