PROBLEM: Neonatal thymectomy (Tx) and estrogen (E2) administration disrupt the reproductive and immune systems of female mice. The current experiment examined the combined effects of the two procedures on ovarian function, performed in sequence, and in reverse sequence. METHOD: Groups of (C57BL/6J x A/J)F1 (B6A) female mice were given four daily injections of 20 micrograms estradiol-17 beta, either from 0 days to 3 days, or from 3 days to 6 days postpartum. In some groups this regimen was combined with thymectomy performed either prior to steroid injection (TX-3), or after steroid treatment (TX-4). Animals were sacrificed between 100 and 110 days of age then ovaries evaluated via light microscopy for dysgenesis and follicular cysts. RESULTS: When E2 treatment followed Tx, the incidence of ovarian dysgenesis was unchanged (study 1, Tx + E2 = 60% ovarian dysgenesis; Tx = 63% ovarian dysgenesis) (study 2, Tx + E2 = 46% ovarian dysgenesis; Tx = 45% ovarian dysgenesis). In contrast, when E2 was given before Tx, ovarian dysgenesis did not occur (study 2, E2 + Tx = 0% ovarian dysgenesis; Tx = 46% ovarian dysgenesis). Ovaries from E2 + Tx animals were characteristic of ovaries from E2-injected animals without Tx. CONCLUSION: The results indicate that E2 injection prevents Tx-induced ovarian dysgenesis, suggesting E2-activation of an extrathymic pathway for thymus function.
PROBLEM: Neonatal thymectomy (Tx) and estrogen (E2) administration disrupt the reproductive and immune systems of female mice. The current experiment examined the combined effects of the two procedures on ovarian function, performed in sequence, and in reverse sequence. METHOD: Groups of (C57BL/6J x A/J)F1 (B6A) female mice were given four daily injections of 20 micrograms estradiol-17 beta, either from 0 days to 3 days, or from 3 days to 6 days postpartum. In some groups this regimen was combined with thymectomy performed either prior to steroid injection (TX-3), or after steroid treatment (TX-4). Animals were sacrificed between 100 and 110 days of age then ovaries evaluated via light microscopy for dysgenesis and follicular cysts. RESULTS: When E2 treatment followed Tx, the incidence of ovarian dysgenesis was unchanged (study 1, Tx + E2 = 60% ovarian dysgenesis; Tx = 63% ovarian dysgenesis) (study 2, Tx + E2 = 46% ovarian dysgenesis; Tx = 45% ovarian dysgenesis). In contrast, when E2 was given before Tx, ovarian dysgenesis did not occur (study 2, E2 + Tx = 0% ovarian dysgenesis; Tx = 46% ovarian dysgenesis). Ovaries from E2 + Tx animals were characteristic of ovaries from E2-injected animals without Tx. CONCLUSION: The results indicate that E2 injection prevents Tx-induced ovarian dysgenesis, suggesting E2-activation of an extrathymic pathway for thymus function.