The submitted collection of papers represents my work in the area of equine ovarian function and dysfunction. During spring transition, the endocrinological events responsible for recruitment of large anovulatory follicles appear to resemble recruitment of preovulatory follicles in the natural breeding season. These large follicles contain only low concentrations of progesterone and oestradiol. They have low expression of mRNA encoding steriodogenic enzymes, have poor development of the theca interna and are poorly vascluarised. These follicles are therefore showing signs of atresia while they are actively increasing in size. In preovulatory follicles, concentrations of inflammatory mediators increase as ovulation approaches, and fluid from preovulatory follicles is chemotactic for leucocytes. Intrafollicular treatment with indomethacin delayed ovulation which supports the central role for inflammation in the ovulatory process. It is also likely the matrix metalloproteinases are involved in the profound tissue remodelling that occurs around ovulation. Control of follicular growth has been studied and equine follicles are dependent on gonadotrophin stimulation when they reach 10 mm in diameter and on LH stimulation for final growth and maturation. The equine CL is dependent, at least in part, on trophic support by LH and luteal cells bind LH in vitro. Steroidogenesis in the CL varies before and after development of the endometrial cups in pregnancy. StAR protein increases after endometrial cup formation, allowing greater mobilisation of substrate for steroid synthesis. Although P450_arom is consistently present in the equine CL, P450_C17 increases after the endometrial cups form, allowing oestrogen synthesis by the CL in the pregnant mare. The cell types in the equine CL appear to co-operate in steriodogenesis, with P450_C17 located in small luteal cells, and P450_arom in large luteal cells. Maintenance of the CL in early pregnancy appears to be caused by the inhibition of endometrial PG synthesis by the conceptus, although the conceptus itself produces PGs. The demise of the CL involves apoptosis and is preceded by a decrease in angiogenesis.