Rat placental lactogens initiate and maintain lactation yet inhibit suckling-induced prolactin release.

Mammalian reproduction is dependent on both a successful pregnancy and on the subsequent period of lactation. In the rat, ovulation occurs shortly after parturition making it possible for a dam to be simultaneously pregnant and lactating. The present studies investigate the effect of placental hormones on suckling-induced prolactin (PRL) release and the contribution of placental hormones to milk synthesis and secretion. A rat choriocarcinoma cell line, Rcho-1, which secretes placental lactogens (PLs) following transplantation in vivo, attenuated suckling-induced PRL release on both d 9 and d 14 of lactation by 43 and 58%, respectively. When PRL secretion was completely inhibited by bromocriptine, a dopamine agonist, Rcho-1-bearing dams still maintained a normal litters weight gain, demonstrating that placental lactogens can continue an established lactation. The Rcho-1 tumors also initiated milk synthesis and secretion in nulliparous rats continuously exposed to pups. Whereas none of the 11 control virgins began lactating and had an average pup weight loss of 2.07 g, the Rcho-1-bearing rats began lactating, as evidenced by a significant reduction in pup weight loss. Thirty percent of these rats became fully lactationally competent. Northern blot analysis showed that the Rcho-1 tumors expressed both PL-I and PL-II mRNA in all experimental groups. These tumors also secreted PL-I into the circulation, as shown by radioimmunoassay.