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  • Title: Estrogen-induced sexual receptivity and localization of 3H-estradiol in brains of female mice: effects of 5 alpha-reduced androgens, progestins and cyproterone acetate.
    Author: Luttge WG, Jasper TW, Gray HE, Sheets CS.
    Journal: Pharmacol Biochem Behav; 1977 May; 6(5):521-8. PubMed ID: 896889.
    Abstract:
    Sexual receptivity induced in ovariectomized CD-1 mice with chronic daily administration of estradiol benzoate (E2 B) was blocked by concurrent administration of the 5 alpha-reduced androgen, dihydrotestosterone (DHT). Receptivity was restored in these females with progesterone-, but not with dihydroprogesterone-priming 6 hr prior to testing. Delaying the DHT injections until 12 hr after the E2 B injections greatly reduced its inhibitory properties. Receptivity in E2 B-primed females was also blocked by concurrent treatment with cyproterone acetate and 3 alpha-, but not 3 beta-adrostanediol. Pretreatment with DHT, or 3 alpha- or 3 beta-androstanediol failed to consistently affects 3H-estradiol accumulation in crude nuclear and supernatant fractions from brain and pituitary. Sexual receptivity induced in ovariectomized CD-1 mice with chronic daily administration of estradiol benzoate (EB; 2 mcg) was investigated and localization of tritiated estradiol in brains of these mice attempted. After 10 days of EB priming dihydrotestosterone (DHT) was given (1 mg/day) and again tested for receptivity. This was followed by further testing after DHT had been stopped. In a 2nd experiment the effect of varying dose and time of administration of DHT on estrogen-induced receptivity was attempted. Dosage of DHT was varied from 500 mcg to 1 mg and time of injection was varied from concurrent with EB injection to 12 hours after. In a 3rd study the effects of DHT, cyproterone acetate (CA), and 3alpha- or 3beta-androstanediol were examined with relation to receptivity. A dosage schedule designed to inhibit receptivity was used. Finally, the effects of DHT and 3alpha- and 3beta-androstanediol on tritiated estradiol localization in brain and pituitary was investigated. Estrogen-induced receptivity was blocked by concurrent administration of the 5aplha-reduced androgen, and DHT. Receptivity was restored in these females with progesterone. However, priming with dihydroprogesterone 6 hours prior to testing was ineffective in restoring receptivity. Delayed DHT injections greatly reduced inhibitory properties. Receptivity was also blocked by concurrent treatment with CA and 3alpha-androstanedio. 3beta-androstanediol was ineffective in blocking receptivity. Pretreatment with DHT or 3alpha- or 3beta-androstanediol failed to affect tritiated estradiol accumulation consistently in crude nuclear and supernatant factions from brain and pituitary.
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