The nonuterotropic metabolite of estradiol, 2-hydroxyestrone, administered at noon of proestrus to four-day cycling rats, abolishes the preovulatory prolactin rise in a large percentage of animals tested. In animals synchronized with exogenous estradiol, 2-hydroxyestrone universally induced a long delay in the prolactin surge. The principal metabolite of 2-hydroxyestrone, 2-methoxyestrone, given at noon of proestrus, significantly augments the magnitude of the preovulatory prolactin rise possibly by inhibiting the formation of endogenous 2-hydroxyestrogens in the brain. The results obtained are consistent with the concept of a physiological function for 2-hydroxyestrogens as estrogen antagonists in the CNS.
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Katayama et al. (1982) studied this question.