Progestins' actions in the VTA to facilitate lordosis involve dopamine-like type 1 and 2 receptors.

In the ventral tegmental area (VTA), 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP) facilitates lordosis. Whether this involves dopamine type 1 (D1) or dopamine type 2 (D2) receptors is of interest. Ovariectomized (ovx) rats with guide cannulae to the VTA were estradiol (E2) primed and pretested for lordosis. Rats were then infused with the D1 (Experiment 1) or D2 (Experiment 2) antagonists or agonists (0, 100, or 200 ng) to the VTA and were retested. After a second infusion of 3alpha,5alpha-THP (0, 100, or 200 ng) or vehicle, rats were tested 10, 60, and 120 min later. In Experiment 3, rats were administered a progestin receptor antagonist, RU38486, systemically or to the VTA 1 h prior to vehicle, SKF38393 and/or 3alpha,5alpha-THP infusions. 3alpha,5alpha-THP infusions increased lordosis over that seen with E2 priming. The D1 antagonist, SCH23390, attenuated 3alpha,5alpha-THP, but not E2-facilitated lordosis. The D1 agonist, SKF38393, augmented 3alpha,5alpha-THP, but not E2-facilitated lordosis. The D2 antagonist, sulpiride, had no significant effects on lordosis. The D2 agonist, quinpirole, prevented 3alpha,5alpha-THP-facilitated lordosis. RU38486 (subcutaneous) inhibited lordosis, whereas infusions to the VTA decreased lordosis produced by SKF38393 and 3alpha,5alpha-THP, but not 3alpha,5alpha-THP alone. Thus, 3alpha,5alpha-THP's actions in the VTA for lordosis may involve D1 and/or D2 receptors.