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However, in contrast to the situation described for rats, the spontaneous activation of rabbit primordial follicles was not inhibited by KITL-neutralizing antibody, suggesting that endogenous KITL does not contribute to the spontaneous activation of primordial follicles in rabbit ovarian cortical explants in vitro. Caution must be applied in the interpretation of these results, as it is possible that this antibody does not inhibit KIT signal transduction in rabbits, as is suggested by our results showing increased rabbit oocyte growth in the presence of combined recombinant KITL protein and neutralizing KITL antibody. In parallel studies with mice, the spontaneous activation of primordial follicles was only partially inhibited by KITL-neutralizing antibody. Therefore, although the endogenous production of KITL may contribute to some spontaneous activation, in the mouse the majority of spontaneous activation appears to be related to some other aspect of the culture system. Possibilities include the provision of exogenous growth factors that follicles are not exposed to under normal physiologic conditions or the absence of an inhibitory substance that is normally present in vivo. In summary, these data indicate that in the rabbit the primary role of KITL is to promote the growth of oocytes during the early stages of development. In contrast, in the mouse, KITL may have a direct role in both primordial follicle activation and promoting oocyte growth and continued follicle development. Only a small percentage of mouse primordial follicles were refractory to both the mediators of spontaneous activation and the recruitment promoting effects of KITL. Why all mouse follicles did not respond in the same way to KITL remains to be elucidated. KITL had no effect on follicle survival for either species. The findings reported here have important implications for the extrapolation of rodent culture systems for the in vitro development of human ovarian follicles.