Research Paper Volume 12, Issue 8 pp 7313—7333

Figure 9. Pharmacological suppression of ER signaling reversibly impairs oogenesis during adulthood. (A) Changes in Stra8 mRNA levels in OSCs cultured with vehicle (V), E2 (10 nM), E2 plus fulvestrant (Ful, 10 nM; E2+Ful), or E2 plus raloxifene (Ral, 10 nM; E2+Ral) for 24 hours (mean ± SEM, n = 3 independent cultures; *P<0.05). (B) Primordial follicle numbers in ovaries of young adult WT mice treated with V, Ful (10 mg/kg), or Ral (20 mg/kg) for 21 days, and 21 days after ceasing Ful or Ral treatment (post-Ful or post-Ral, respectively) (mean ± SEM, n = 7–13 mice per group; *P<0.05). (C–E) Numbers of recently growth-activated (primary; C) and early growing (small-preantral; D) immature follicles, and of degenerative oocytes (E), in ovaries of WT mice treated as described in panel B (mean ± SEM, n = 7–13 mice per group; *P<0.05). (F) Changes in ovarian Stra8 mRNA levels in WT mice treated as described in panel B (mean ± SEM, n = 7–13 mice per group; *P<0.05). (G) Schematic depiction of how reversible ER antagonists likely alter oocyte dynamics in adult ovaries by transiently disrupting endogenous E2-promoted OSC differentiation into new oocytes, yielding a net decline in total oocyte numbers due to attenuated input that then fully recovers after ceasing ER antagonist exposure.