Although recent studies in other laboratories have greatly increased our understanding of luteal function in cattle, we are still unable to accurately synchronise luteolysis, preovulatory follicular growth and ovulation with commercially available pharmacological preparations. The aim of these studies was to investigate the factor(s) which controls the formation, function and regression of the GnRH-induced corpus luteum (CL). Initially, we sought to develop an experimental model to examine the characteristics of the CL induced in intact heifers with normal oestrous cyclicity, by GnRH injection in the early luteal phase. Administration of GnRH on Day 6 after the synchronised oestrus resulted in ovulation and formation of an additional CL in >70% of animals. Following prostaglandin F_2α(PGF_2α) in the mid-luteal phase, the spontaneously-formed CL underwent luteolysis while the induced CL did not, leading to a delay in return to oestrus associated with a persistence of luteal function. Having demonstrated the ovulatory competence of the dominant follicle of the first follicular wave, and the formation of a functional CL, it was of interest to examine the reason for the premature demise of the induced CL in the GnRH responders when compared to the spontaneously-formed CL. Administration of steroid-stripped bovine follicular fluid (bFF), which suppressed the growth of the dominant follicle, and reduced serum oestradiol concentrations, resulted in a further delay in the return to oestrus and a significant extension in the lifespan of the induced CL, when compared to the untreated responders, and provided circumstantial evidence that oestradiol was the endogenous agent responsible for regression of the induced CL.