Exogenous gonadotrophin (eg. PMSG) treatment results in follicular growth in most reproductive states, and suggests that lack of FSH and LH-like activity is a likely cause of arrested-follicular development in the pig. Endogenous changes in gonadotrophins between reproductive and non-reproductive states are consistent with this concept. However, changes in the pattern of LH secretion, rather than clearly defined changes in FSH release, appear to be the effective trigger for follicular recruitment. In other situations in vivo, follicular growth is initiated in the absence of demonstrable changes in LH or FSH secretion, suggesting that other hormones interact to sensitize the ovary to gonadotrophins. Such effects have been reported for insulin, cortisol, thyroxine and IGF-1 in vitro, and the steroid environment of follicles also affects gonadotrophin receptors and receptor-mediated mechanisms. Once initiated, the regulation of follicle maturation also involves interactions between gonadotrophins and steroids, as well as other intra-ovarian regulators. Co-operation exists between theca and granulosa in the synthesis of steroids and androgen precursor availability is an important regulator of the oestrogenic activity of follicles. Considerable heterogeneity exists in the morphological and biochemical maturity of preovulatory follicles and inter-follicular regulation via endocrine and paracrine mechanisms may be an essential component of the selection process.