on the pattern of suckling unless there exists refractoriness or some other form of non-linearity in the mechanism of prolactin synthesis and release. A possible theoretical base for understanding this problem has been given by the experimental work or Charles Grosvenor and his associates at the university of Tennessee. Grosvenor's group found that a metabolite of TRH, cylco-his-pro, inhibits the transformation of prolactin in the pituitary from a pre-releasable to a releasable form. They theorise that TRH released by the hypothalamus in response to the suckling inhibits the release of dopamine from the TIDA (tubero-infundibular dopaminergic) neurones of the hypothalamus, thus removing the chronic inhibition of the transformation of prolactin from its pre-releasable to its releasable form. However, TRH is quickly metabolised, yielding cyclo-his-pro that blocks further transformation. After an interval has elapsed between suckling bouts, the refractory state abates. A new suckling stimulus then is capable of triggering another prolactin release and an additional prolactin transformation in preparation for the next stimulus-release episode.h Hormonal Responses not Mediated by Prolactin McNeilly et al. proposed the existence of a GnRH (gonadotrophin releasing hormone) pulse generator located in the hypothalamus that can be disrupted by input from the mammary nerve when stimulated by suckling. This disruption would depress reproduction since pulsatile secretion of GnRH is necessary for the development of the episodic release and eventual surge in LH (lutienizing hormone) secretion. The LH surge is considered to be the necessary trigger for rupture of the ripened ovarian follicle, i.e. ovulation. In their view, the suckling stimulus is the key factor in the endocrine control of lactational infertility and anything that undermines or reduces this stimulus will result in as resumption of ovarian activity with a variable return in ferti...
