CENTRAL LACTOGENIC REGULATION OF MATERNAL-BEHAVIOR IN RATS - STEROID DEPENDENCE, HORMONE SPECIFICITY, AND BEHAVIORAL POTENCIES OF RAT PROLACTIN AND RAT PLACENTAL-LACTOGEN .1.

Citation
Rs. Bridges et al., CENTRAL LACTOGENIC REGULATION OF MATERNAL-BEHAVIOR IN RATS - STEROID DEPENDENCE, HORMONE SPECIFICITY, AND BEHAVIORAL POTENCIES OF RAT PROLACTIN AND RAT PLACENTAL-LACTOGEN .1., Endocrinology, 138(2), 1997, pp. 756-763
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
138
Issue
2
Year of publication
1997
Pages
756 - 763
Database
ISI
SICI code
0013-7227(1997)138:2<756:CLROMI>2.0.ZU;2-E
Abstract
Adult virgin female rats display maternal behavior when continuously e xposed to foster young for 5-6 days. Central infusions of PRL or place ntal lactogens (PLs) together with systemic treatment of progesterone (P) and estradiol (E(2)) stimulate maternal behavior in 1-2 days. In t he present set of studies, it was asked whether the actions of lactoge nic hormones are dependent upon both E(2) and P and specific to lactog enic molecules. Moreover, we wanted to know whether central infusions of rat (r) PRL and PLs were equally effective in inducing maternal beh avior. In the first study, adult virgin rats were ovariectomized (ovx) and stereotaxically fitted with bilateral cannulas directed at the me dial preoptic area (MPOA). Rats were then assigned to one of four grou ps: P plus E(2), blank (B) plus E(2), P plus B, and B plus B. P-filled or B capsules were implanted sc on treatment day 1 and removed on day 11, whereas E(2) or B capsules were implanted on day 11. All groups w ere infused with rPRL (40 ng/side) five times from days 11-13 and inje cted with bromocriptine (CB-154) sc (days 11-17) to suppress endogenou s PRL release. Behavioral testing was conducted daily from days 12-17. It was found that exposure to both P and E(2) was necessary to induce a fast onset of maternal behavior in PRL-infused females; priming wit h P or E(2) alone in PRL-treated rats failed to stimulate a fast onset of behavior relative to that in nonsteroid-treated controls. In the s econd experiment to determine the biochemical specificity of PRL's act ion, adult nulliparous rats were ovx, implanted with bilateral cannula s directed at the MPOA, treated with both P and E(2), injected with CB -154, and infused centrally (five times) with 40 ng (per side) of bovi ne GH, ovine LH, or vehicle. Central infusions of either bovine GH or ovine LH failed to stimulate maternal behavior, suggesting that the st imulatory actions of PRL are related to its lactogenic properties. In the final study, rats were ovx, fitted with bilateral cannulas directe d at the MPOA; treated with P, E(2), and CB-154; and given a single se t of bilateral infusions of rPL-I or rPRL (40 ng/side infusion) on day 11, three sets of infusions of rPL-I or rPRL (days 11 and 12), or veh icle infusions. Rats given three infusions of rPL-I and rPRL responded faster than controls, although the effect was not as robust as that i n animals given five infusions in the initial study. rPL-I and rPRL gr oups did not differ from one another. Together these studies indicate that 1) both P and E(2) are required for lactogenic stimulation of mat ernal behavior; 2) the stimulatory actions of PRL and rPLs on maternal behavior are related to their lactogenic properties; 3) extended trea tment of females with lactogenic hormones is more effective in stimula ting the onset of maternal behavior; and 4) the neural potencies of rP RL and rPL-I are similar. These findings provide support for the idea that the induction of maternal behavior is stimulated by the central a ctions of lactogenic hormones.