Is GnRH self-priming an obligatory feature of the reproductive cycle?

Insufficient suppression of LH (premature elevation) and FSH (prolonged rel ease) give rise to blood concentrations which may cause damaging effects on oocyte viability and too many follicles respectively. During the surge, LH rises from low to high threshold values to initiate processes from initiat ion of the resumption of oocyte meiosis to the induction of ovulation. In g eneral, it is thought that a dramatic increase in LH concentration is requi red to attain the high threshold for ovulation. A self-priming mechanism, b y which gonadotrophin-releasing hormone (GnRH) enhances the LH (and FSH) re sponses to its own action, was thought to be responsible. However, normal L H surges in rats consist of <2-7% of the maximal pituitary releasing capaci ty. The physiological roles of LH and FSH favour a control mechanism that r estrains their blood concentrations during most of the cycle. Ovarian prote ins, e.g. inhibin and putative gonadotrophin-surge-inhibiting factor/attenu ating factor (GnSIF/AF), are involved in this process. We argue that the in creased pituitary LH responsiveness during the mid-cycle surge is not the r esult of a self-priming process that 'dramatically' increases the LH releas ing capacity of the pituitary gland. This is probably due to elimination by GnRH of the inhibitory action of the putative ovarian proteins GnSIF/AF.