SR 27417 Therefore, these results suggest that AMH improves oocytes quality by up-regulating GDF9 and BMP15 mRNA expressions during IVM. Studies have shown that AMH expression is strongest in preantral and small antral follicles, and then decreases continually. AMHR-II is co-expressed with AMH in granulosa cells of growing follicles. In rat and sheep, AMH and AMHR-II are specifically expressed in granulosa cells, and there is no expression in the oocytes, theca and interstitial cells or expressed very little amount of AMH and AMHR-II in those cells. Interestingly, our results indicated that AMH mRNA expression and protein only localized in cumulus cells. However, AMHR-II mRNA expression and protein were localized at both oocyte and cumulus cells. AMH may have effects on both cumulus cells and oocytes through autocrine and paracrine when COCs were cultured in vitro. In rat and sheep, the expression of AMHR-II was not observed in the oocytes from antral follicles. Therefore, the different observations could be due to technical variations between the studies or due to different species. In addition, as AMHR-II is a membrane receptor, using immunocytochemical method may not detect AMHR-II expression, because the cell membranes, especially large cells like oocytes, it may not be integrated properly in these studies. It has been reported that another member of TGF-b superfamily, BMP receptor IB is located at both oocyte and granulosa cells in sheep ovary. Same as sheep ovary, AMHR-II may be similar to this TGF-b superfamily receptor in mouse COCs. However, Sedes L et al. found that AMH could recruit BMPR-IA in immature granulosa cells. Therefore, further study is required to confirm the linkage of those two receptors. Belonging to the TGF-b superfamily, GDF9 and BMP15 play crucial roles in the follicular development, ovulation, oocyte maturation, and embryo development, and they are essential factors for folliculogenesis and female fertility. It has been reported that GDF9 and BMP15 are closely associated with oocyte quality and embryo Retro-2 developmental potential. In GDF9-deficient female mice, the ultrastructure of oocytes is abnormal; ovulation and oocyte fertilization rate are decreased in BMP15 knock-out model.