Induced follicular atresia in rhesus monkeys: strength-duration relationships of the estrogen stimulus

• Published in: Endocrinology (Philadelphia) Vol. 117; no. 4; p. 1397
• Main Authors: Dierschke, D J, Hutz, R J, Wolf, R C
• Format: Journal Article
• Language: English
• Published: United States 01-10-1985
• Subjects: Animals; Delayed-Action Preparations; Estradiol - administration & dosage; Estradiol - pharmacology; Estrogens - blood; Female; Follicle Stimulating Hormone - blood; Follicular Atresia - drug effects; Follicular Phase - drug effects; Luteinizing Hormone - blood; Macaca mulatta; Menstrual Cycle - drug effects; Progesterone - blood; Time Factors
• ISSN: 0013-7227
• DOI: 10.1210/endo-117-4-1397

We have demonstrated that 17 beta-estradiol (E2) administered to monkeys for 24 or 48 h from day 6 of the menstrual cycle results consistently in degeneration of the preovulatory follicle. The present experiments were conducted to determine the strength-duration characteristics of this effect and to evaluate the occurrence of partial atresia together with subsequent effects on luteal function. Square wave increments in circulating amounts of estrogen were achieved by varying the number and size of Silastic capsules containing E2. Treatments included 0.5, 1, 2, 4, or 10 capsules placed sc for 6, 12, or 24 h. Forty-six menstrual cycles were studied in 33 animals. Increments in serum concentrations of estrogen approximating 300-400 pg/ml and sustained for 24 h or those greater than 600 pg/ml for only 6 h were maximally effective, while 300-400 pg/ml for 12 h or 100 pg/ml for 24 h were almost as effective. Increments less than about 60 pg/ml were essentially ineffective in inducing atresia. After induced atresia, follicular phases were extended by about 8 days, permitting a substitute follicle to develop. Partial atresia, represented by delayed ovulation of the original follicle, was noted in only three cycles. However, another apparent effect of estrogen on follicular development was evident in the form of luteal phase defects which occurred with high incidence in all groups, whether the corpus luteum resulted from the original or substitute follicle. Thus, full atresia induced by estrogen is largely an all or none phenomenon, but lesser effects may be manifested as deficient luteal function. This atretogenic effect of estrogen may be exerted at the ovarian level or may be mediated by the transient suppression of FSH. On the other hand, increases in FSH after treatment may stimulate development of a substitute follicle or maintain follicles not undergoing full atresia.