A Possible Mechanism for the Induction of Lordosis by Reserpine in Spayed Rats

• Published in: Biology of reproduction Vol. 4; no. 1; pp. 23 - 30
• Main Authors: Paris, C A, Resko, J A, Goy, R W
• Format: Journal Article
• Language: English
• Published: United States Society for the Study of Reproduction 01.02.1971
• Subjects: Adrenal Glands - metabolism; Animals; Castration; Dexamethasone - pharmacology; Estradiol - pharmacology; Female; Hypophysectomy; Metyrapone - pharmacology; Mice; Ovary - physiology; Pituitary Gland - physiology; Posture; Progesterone - metabolism; Reserpine - pharmacology; Sexual Behavior, Animal - drug effects
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1093/biolreprod/4.1.23

In the ovariectomized, estrogen-primed rat the injection of reserpine was associated with the display of lordosis and an increase in the concentration of progesterone in systemic plasma. Following injection of 0.5 mg reserpine, 100% of the animals displayed the lordosis reflex and the median concentration of progesterone in the plasma was 4.6 ng/ml. In estrogen-primed controls injected with vehicle, only 30% of the females displayed lordosis and the median progesterone concentration was 1.4 ng/ml. When estrogen-primed rats were treated with dexamethasone, a corticotropin suppressor, reserpine neither facilitated lordosis nor induced a rise in plasma concentration of progesterone. The incidence and character of lordosis following progesterone injection, however, were not changed by treatment with dexamethasone. Hypophysectomy prevented the elevation of plasma progesterone following reserpine. All animals studied ( N = 4) showed nondetectable concentrations of progesterone. When Metopirone, a corticotropin activator, was given to estrogen-primed, spayed rats, the percentage showing lordosis (78%) and the median concentration of progesterone (4.2 ng/ml) were not significantly different from those found following reserpine. Just as with reserpine, moreover, neither of these effects occurred when dexamethasone was given prior to Metopirone. The results suggest that reserpine influences lordosis not by acting directly on the neural tissues regulating this behavior, but indirectly by stimulating release of ACTH; progesterone and possibly other physiologically relevant steroids which induce lordosis are presumed to be secreted by the adrenals in response to this ACTH release. A similar mechanism may permit reserpine to inhibit or facilitate gonadotropin release and stimulate prolactin production.