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