Prolactin and estradiol increase striatal dopamine receptor density in intact, castrated and hypophysectomized rats.

1. Ovariectomized female or intact male rats were implanted with three adenohypophyses under the kidney capsule or treated with 17 beta-estradiol (10 micrograms twice daily) for 2 weeks. 2. In animals of both sexes, the pituitary-implanted and estradiol-treated rats had elevated plasma prolactin levels and had increased levels of striatal dopamine receptors. 3. We next investigated the possibility of an indirect action of estradiol via prolactin using hypophysectomized female rats (hypox) treated with 17 beta-estradiol or ovine prolactin (500 micrograms, twice daily) for 5 days. 4. Striatal dopamine receptor concentration was lower in hypox animals as compared to ovariectomized (85%, p less than 0.05) or intact female rats at random stage of the estrous cycle (76%, p less than 0.05) while the affinity (KD) of [3H]spiperone for these dopaminergic sites remained unchanged. 5. Treatment with estradiol or prolactin increased the level of striatal dopamine receptors (HYPOX + estradiol: 144% vs HYPOX, p less than 0.05; HYPOX + prolactin: 147% vs HYPOX, p less than 0.05). 6. These results indicate that high prolactin levels induced by pituitary implants or by injections of ovine prolactin lead, as observed with chronic estradiol treatment, to an increased density of striatal dopamine receptors. However, the effect of estradiol may not be explained exclusively by increased prolactin levels since the supersensitivity is also observed in hypophysectomized animals.