Mammary glands from lactating and non-lactating post-partum rats were assayed for prolactin (PRL) and estradiol (E2) binding sites. In lactating animals serum PRL and tissue E2 and PRL binding increased rapidly in the first 2 days post-partum and thereafter declined until day 15 to 20 post-partum. In non-lactating rats in the postpartum period, no comparable changes in the three parameters were observed. Hysterectomy of pregnant rats on day 21 was followed by an increase in serum PRL concentrations but no increase in mammary tissue binding of PRL or E2 was found. Similar results were observed after hysterectomy and oophorectomy except no increase in serum PRL was noted. The administration of estradiol to the mother immediately after birth decreased mammary tissue PRL binding sites, while the administration of hydroxyprogesterone decreased binding of E2 but left PRL binding unchanged. Post-partum suppression of PRL secretion with Bromocriptin decreased PRL but not E2 binding and, in addition, decreased weight gain of the pups. The changes caused by Bromocriptin were partially reversed by the simultaneous administration of oPRL during the treatment period. The data presented indicate that mammary gland PRL receptors are increased by PRL and thus exhibit the same autoregulation noted previously in the liver. Estrogens, which increase hepatic PRL binding, exert an opposite effect on mammary gland PRL receptors. The increase in serum PRL at the end of gestation is in part dependent on the presence of ovaries and the suckling stimulus causes a further increase.
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Bohnet et al. (1977) studied this question.
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