Posterior pituitary lobectomy abolishes the suckling-induced rise in prolactin (PRL): evidence for a PRL-releasing factor in the posterior pituitary.Endocrinology. 1987 Jul; 121(1):205-11.E
The aim of this study was to determine the role of the posterior pituitary in the regulation of PRL release during suckling. Lactating rats were subjected to posterior pituitary lobectomy (LOBEX) or sham surgery (SHAM) and separation from pups in the evening; experimental manipulations and blood collection were performed the next morning. In the first experiment rats were divided into three groups: SHAM, LOBEX, and LOBEX treated with a vasopressin analog, 1-desamino-8-D-arginine vasopressin and oxytocin. Plasma PRL levels in SHAM rats increased 20- to 25-fold upon introduction of pups and remained elevated for the duration of suckling. In contrast, basal plasma PRL levels in LOBEX rats were 3- to 4-fold higher than in SHAM but suckling failed to induce a further increase. Treatment of LOBEX rats with 1-desamino-8-D-arginine vasopressin and oxytocin reduced water consumption and allowed for milk ejection and milk intake by the pups but did not restore the suckling-induced rise in PRL. The second experiment tested the functional integrity of the hypothalamic dopamine (DA) and serotonergic systems after LOBEX and the ability of LOBEX-lactating rats to respond to PRL-releasing stimuli other than suckling. Injections of alpha-methyl-para tyrosine, an inhibitor of tyrosine hydroxylase, and 5-hydroxytryptophan, a precursor of serotonin, caused 20- to 30-fold rises in plasma PRL levels in both LOBEX and SHAM rats. Exposure to ether elicited a 3- to 4-fold rise in PRL which was higher in magnitude and of longer duration in LOBEX than in SHAM rats.
Removal of the posterior pituitary from lactating rats results in an increase in basal PRL levels and a complete abolishment of the suckling-induced rise. Vasopressin and oxytocin restore water balance and milk ejection in the LOBEX rat but fail to affect PRL secretion. The LOBEX-lactating rat is not refractory to PRL-releasing stimuli other than suckling and its hypothalamic DA and serotonergic systems are functionally intact. In addition to DA, the posterior pituitary appears to contain a PRL-releasing factor(s) which mediates the suckling-induced rise in PRL.