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Epiallopregnanolone, a endogenous 3 β-isomer of allopregnanolone, is a metabolite of progesterone. Epiallopregnanolone is a competitive antagonist at the neurosteroid site on the GABAA receptor [1]. GABAA receptors are GABA -gated chloride channels involved in mediating neuronal inhibition in the brain [2].

In vitro: Epiallopregnanolone showed no effects on the GABA-mediated chloride flux through several types of recombinant GABA receptors. Epiallopregnanolone inhibited the allopregnanolone-stimulated GABA-mediated chloride flux through GABAA receptors. Epiallopregnanolone antagonized the inhibitory effects of allopregnanolone and ethanol on the population spike in the CA1 region of the hippocampal brain slices [1]. Epiallopregnanolone selectively blocked the allopregnanolone inhibition of the population spike in the rat hippocampal CA1[3].

In vivo: In rats trained to discriminate either 0.8g/kg or 1.2 g/kg ethanol, 100 mg/kg epiallopregnanolone treatment decreased the maximum effect by 40% and 54% ethanol lever, respectively. Epiallopregnanolone significantly decreased response rates when compared with control condition [1].

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