Evidence for direct inhibition of ovarian function by prolactin.

There is no doubt that in breast-feeding women, suckling with its associated hyperprolactinaemia prevents the resumption of ovarian activity for prolonged periods (see McNeilly, 1979). The extent of this suppression varies greatly among species but in all for which there are adequate data it appears to depend critically upon the intensity of the suckling stimulus (Lamming, 1978). Our recent data from women show that in the pattern of suckling, frequency and duration, throughout the day, are both key factors in maintaining the elevation of basal levels of prolactin associated with lactation (McNeilly, Howie & Houston, 1980a; Howie & McNeilly, 1982). Suckling also releases large quantities of prolactin, maintaining a physiological hyperprolactinaemic state which is directly associated with the duration of lactational amenorrhoea (Delvoye, Badawi, Demaegd & Robyn, 1978; Duchen & McNeilly, 1980). The question remains, how does suckling suppress ovarian activity? The levels of prolactin in blood during peak lactation appear to be many times the requirement for production of milk. It therefore becomes pertinent to ask whether this prolactin is released solely to stimulate milk production or whether it is involved directly in the suppression of ovarian activity. If there is a direct involvement then there are two loci for this action; an effect at the hypothalamic-pituitary level or a direct effect on the ovary. While the former has received some attention (see McNeilly, 1979, 1980a), relatively little information is available (for species other than the rat) on whether or how prolactin might act on the ovary and, in particular, how high levels might interfere or block follicular development during lactation (McNeilly, 1980b). The purpose of this paper is to review the evidence for a direct action of prolactin on the ovary in the context of the effects of prolactin in the control of normal ovarian cyclicity.