| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Articles |
Department of Comparative Medicine (R.S.B., J.D.S., B.M.H., P.E.M.), Tufts University School of Veterinary Medicine, North Grafton, Massachusetts 01536; and the Department of Physiology (M.C.R., R.P.C.S.), University of Manitoba School of Medicine, Winnipeg, Manitoba, Canada R3E 0W3
Address all correspondence and requests for reprints to: Robert S. Bridges, Ph.D., Department of Comparative Medicine, Peabody Pavilion, Tufts University School of Veterinary Medicine, 200 Westboro Road, North Grafton, Massachusetts 01536. E-mail: RBRIDGES{at}INFONET.TUFTS.EDU
Adult virgin female rats display maternal behavior when continuously exposed to foster young for 5–6 days. Central infusions of PRL or placental lactogens (PLs) together with systemic treatment of progesterone (P) and estradiol (E2) stimulate maternal behavior in 1–2 days. In the present set of studies, it was asked whether the actions of lactogenic hormones are dependent upon both E2 and P and specific to lactogenic molecules. Moreover, we wanted to know whether central infusions of rat (r) PRL and PLs were equally effective in inducing maternal behavior. In the first study, adult virgin rats were ovariectomized (ovx) and stereotaxically fitted with bilateral cannulas directed at the medial preoptic area (MPOA). Rats were then assigned to one of four groups: P plus E2, blank (B) plus E2, 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 E2 or B capsules were implanted on day 11. All groups were infused with rPRL (40 ng/side) five times from days 11–13 and injected with bromocriptine (CB-154) sc (days 11–17) to suppress endogenous PRL release. Behavioral testing was conducted daily from days 12–17. It was found that exposure to both P and E2 was necessary to induce a fast onset of maternal behavior in PRL-infused females; priming with P or E2 alone in PRL-treated rats failed to stimulate a fast onset of behavior relative to that in nonsteroid-treated controls. In the second experiment to determine the biochemical specificity of PRL’s action, adult nulliparous rats were ovx, implanted with bilateral cannulas directed at the MPOA, treated with both P and E2, injected with CB-154, and infused centrally (five times) with 40 ng (per side) of bovine GH, ovine LH, or vehicle. Central infusions of either bovine GH or ovine LH failed to stimulate maternal behavior, suggesting that the stimulatory actions of PRL are related to its lactogenic properties. In the final study, rats were ovx, fitted with bilateral cannulas directed at the MPOA; treated with P, E2, and CB-154; and given a single set 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 vehicle infusions. Rats given three infusions of rPL-I and rPRL responded faster than controls, although the effect was not as robust as that in animals given five infusions in the initial study. rPL-I and rPRL groups did not differ from one another.
Together these studies indicate that 1) both P and E2 are required for lactogenic stimulation of maternal behavior; 2) the stimulatory actions of PRL and rPLs on maternal behavior are related to their lactogenic properties; 3) extended treatment of females with lactogenic hormones is more effective in stimulating the onset of maternal behavior; and 4) the neural potencies of rPRL and rPL-I are similar. These findings provide support for the idea that the induction of maternal behavior is stimulated by the central actions of lactogenic hormones.
This article has been cited by other articles:
 |
|
 |
|
  R. Arumugam, D. Fleenor, and M. Freemark Lactogenic and Somatogenic Hormones Regulate the Expression of Neuropeptide Y and Cocaine- and Amphetamine-Regulated Transcript in Rat Insulinoma (INS-1) Cells: Interactions with Glucose and Glucocorticoids Endocrinology, January 1, 2007; 148(1): 258 - 267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Numan Hypothalamic neural circuits regulating maternal responsiveness toward infants. Behav Cogn Neurosci Rev, December 1, 2006; 5(4): 163 - 190. [Abstract] [PDF]
|
|
|
|
|
|
G. M. Anderson, D. R. Grattan, W. van den Ancker, and R. S. Bridges Reproductive Experience Increases Prolactin Responsiveness in the Medial Preoptic Area and Arcuate Nucleus of Female Rats Endocrinology, October 1, 2006; 147(10): 4688 - 4694. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Hoshino, Y. Wakatsuki, M. Iigo, and S. Shibata Circadian Clock Mutation in Dams Disrupts Nursing Behavior and Growth of Pups Endocrinology, April 1, 2006; 147(4): 1916 - 1923. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. C. Gammie Current Models and Future Directions for Understanding the Neural Circuitries of Maternal Behaviors in Rodents Behav Cogn Neurosci Rev, June 1, 2005; 4(2): 119 - 135. [Abstract] [PDF]
|
|
|
|
|
|
M. Tanaka, Y. Hayashida, T. Iguchi, N. Nakao, M. Suzuki, N. Nakai, and K. Nakashima Identification of a Novel First Exon of Prolactin Receptor Gene Expressed in the Rat Brain Endocrinology, June 1, 2002; 143(6): 2080 - 2084. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. Grattan, J. Xu, M. J. McLachlan, I. C. Kokay, S. J. Bunn, R. C. Hovey, and H. W. Davey Feedback Regulation of PRL Secretion Is Mediated by the Transcription Factor, Signal Transducer, and Activator of Transcription 5b Endocrinology, September 1, 2001; 142(9): 3935 - 3940. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Bole-Feysot, V. Goffin, M. Edery, N. Binart, and P. A. Kelly Prolactin (PRL) and Its Receptor: Actions, Signal Transduction Pathways and Phenotypes Observed in PRL Receptor Knockout Mice Endocr. Rev., June 1, 1998; 19(3): 225 - 268. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
