A series of experiments were conducted to determine whether and under what conditions central prolactin (PRL) administration would stimulate the onset of maternal behavior in female rats and to identify possible neural sites of PRL action. In each experiment ovariectomized, nulliparous rats whose endogenous PRL levels were suppressed with bromocriptine were tested for maternal behavior toward foster young. In experiments 1, 2, and 4, females were also exposed to pregnancy-like levels of progesterone (days 1-11) followed by estradiol (days 11-17). In experiment 1 infusions (days 11-13) of four doses of ovine PRL (400 ng, 2 ,ug, 10 ,ug, or 50 jug, but not 80 ng) into the lateral ventricle resulted in a rapid onset of maternal behavior (behavioral testing, days 12-17). The stimulatory action of these doses of PRL appears to be central, since subcutaneous injections of 50 jug of ovine PRL failed to affect maternal responsiveness (experiment 2). Experiment 3 indicated that the stimulatory effect of intracerebroventricularly administered PRL is steroid dependent. Infusions of either 10 ,ug of ovine PRL or 10 1ug of rat PRL failed to induce maternal behavior in nonsteroid-treated animals. In the final experiment (no. 4) bilateral infusions of 40 ng of ovine PRL into the medial preoptic area of steroid-treated rats resulted in a pronounced stimulation of maternal behavior. These findings demonstrate a central site of PRL action in the stimulation of maternal responsiveness and point to the medial preoptic area as a key neural site for PRL regulation of maternal behavior.The hormonal changes accompanying pregnancy and parturition play a critical role in preparing the female to respond maternally toward her newborn young (1-4). One hormone that recently was shown to have a key role in inducing maternal behavior is the pituitary hormone prolactin (PRL) (5, 6). PRL and other members of the PRL family-i.e., growth hormone and placental lactogens-are secreted in large amounts during pregnancy (7-9), making these molecules potential physiological regulators of maternal behavior. Eliminating or suppressing PRL secretion in steroid-treated, ovariectomized, nulliparous rats by either hypophysectomy or administration of bromocriptine, a dopamine agonist, blocks the rapid onset of maternal behavior (5, 6). These effects are prevented when PRL is given to hypophysectomized or bromocriptine-treated female rats.Although PRL stimulates the onset of maternal behavior, little is known about PRL's site of action. The purpose of the present report was to investigate the possibility that PRL acts at the level of the central nervous system to stimulate maternal behavior. A central site of PRL action is feasible in light of a series of findings that indicate that circulating PRL can gain access to the brain through active transport across the blood-cerebrospinal fluid (CSF) barrier (10), that PRL, presumably of pituitary origin, is found in increased amounts within the CSF at times when circulating levels of PRL are elevated (11-13), ...

The possible role of the conceptus in stimulating the onset of maternal behavior through its secretion of placental lactogens and their passage into the brain was investigated in female rats. In the first study, significant mitogenic activity in the Nb₂ lymphoma cell bioassay was detected in cerebrospinal fluid (CSF) samples collected by push-pull perfusion from rats on days 12–21 of pregnancy, coincident with the establishment of placental function. In contrast, mitogenic activity was absent from CSF in lactating and gonadectomized, virgin females. In a second study the mitogenic activity in day 12 pregnant samples was neutralized 71% with antibodies to rat placental lactogen-I (rPL-I) and > 90% with a combination of antibodies to rPL-I plus rPL-II. In contrast, activity on day 21 of pregnancy, 1 day prepartum, was reduced by antibodies to rPL-II (>85%), but not by antibodies to rPL-I, indicating that the predominant lactogen in the CSF prepartum is rPL-II. The behavioral actions of placental secretions were assessed in the third experiment by infusing recombinant rPL-I and purified rPL-II directly into the medial preoptic area of the brain of steroid-primed, nulliparous rats. Latencies to respond maternally to foster young were significantly reduced in rPL-I- and rPL-II-treated rats (2- to 3-day latencies) when compared with latencies in control females (5- to 6-day latencies). Thus, the conceptus through its secretion of rPLs which apparently gain access to the CSF helps to prime the pregnant female’s brain to respond maternally at the end of gestation. This endocrine communication between the developing conceptus and pregnant female appears to be an important part of the biological system which helps to establish successful maternal care.

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