Estradiol accelerates extinction of a conditioned taste aversion in female and male rats

Exogenous testosterone treatment prolongs extinction of conditioned taste aversions and estradiol treatment prevents testosterone from prolonging extinction in both gonadectomized males and females. Estradiol could require the presence of testosterone for its effect or its action alone could accelerate extinction. The first series of experiments were designed to test the hypothesis that estradiol accelerates extinction when it is given in the absence of testosterone. The results showed that estradiol accelerates extinction of conditioned taste aversions in the absence of testosterone in gonadectomized Sprague-Dawley females and Fischer 344 females and males. The second series of experiments were designed to determine whether estradiol and testosterone differ in the temporal requirements for their opposite effects on extinction. The results showed that estradiol can accelerate extinction when it is present before and during acquisition (from 8 days before until 3 days after acquisition) or when it is present before and during extinction (from 2 days after acquisition, which was 23 days before extinction, until extinction trials were terminated). This is in contrast to a previous finding that testosterone prolongs extinction only when it is present before and during extinction. The following two hypotheses were suggested to account for the temporal effects of estradiol ain extinction of conditioned taste aversions: (1) the presence of estradiol during acquisition reduces the effectiveness of LiCl through its action on the opioid system, and the presence of estradiol during extinction activates a neural pathway, such as that associated with activity levels, that accelerates extinction of passive avoidance tasks in general or (2) the presence of estradiol before, not during, acquisition or extinction accelerates extinction because of its illness-inducing properties. Most of the evidence supports the second hypothesis. (C) 1999 Academic Press.