Luttge W G, Jasper T W, Gray H E, Sheets C S
Pharmacol Biochem Behav. 1977 May;6(5):521-8. doi: 10.1016/0091-3057(77)90111-3.
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.
长期每日给去卵巢的CD-1小鼠注射苯甲酸雌二醇(E2B)诱导的性接受能力,会被同时注射5α-还原雄激素双氢睾酮(DHT)所阻断。在测试前6小时用孕酮预处理这些雌性小鼠可恢复其性接受能力,但用双氢孕酮预处理则不能。将DHT注射推迟到E2B注射后12小时,可大大降低其抑制作用。同时用醋酸环丙孕酮和3α-雄烷二醇(而非3β-雄烷二醇)处理,也会阻断E2B预处理雌性小鼠的性接受能力。用DHT、3α-或3β-雄烷二醇预处理,未能始终如一地影响来自脑和垂体的粗核及上清液组分中3H-雌二醇的积累。