| Abstract: | A new model for the investigation of atresia in rhesus monkeys is presented. This model is based upon the reliable induction of an atresia-like process in the dominant preovulatory follicle (DF) by estradiol-17 beta administered subcutaneously via Silastic capsules for 24 h. Data obtained from follicular contents aspirated from treated animals demonstrated alterations in the putative markers of atresia similar to those described in other models of atresia. Although follicle size and appearance and volume of follicular fluid (FF) were unaltered in treated animals, FF was much more viscous than that aspirated from follicles in untreated animals; this was apparently due to a greater quantity of intercellular matrix that was sensitive to digestion by hyaluronidase. In treated animals, FF concentrations of estrogen (E) and progesterone (P) were depressed 3- and 6.6-fold, respectively. Viability of granulosa cells (GC) from these animals was reduced by 40%, as was their ability to release basal amounts of E and P in vitro. Accumulation of P by GC from treated animals approximated unstimulated control levels when human follicle-stimulating hormone (hFSH) was included in the culture. Therefore, FSH may have a limited capability to "rescue" GC from atresia induced by estradiol. The percentage of cells that bound 125I-hFSH maximally, as measured by autoradiography following 72 h in culture, was not altered by treatment. Oocytes from animals treated with estradiol showed signs of degeneration at aspiration, and deteriorated further in culture. This model is unique in that atresia can be induced in the single DF of a primate species, and thus avoids the disadvantages inherent to studying atresia of heterogeneous follicles in polytocous species.(ABSTRACT TRUNCATED AT 250 WORDS) |
