NULL MUTATION OF THE PROLACTIN RECEPTOR GENE PRODUCES A DEFECT IN MATERNAL-BEHAVIOR

We have studied pup-directed maternal behavior in mice carrying a germ line null mutation of the PRL receptor (PRLR) gene. Homozygous mutant and heterozygous mutant nulliparous females show a deficiency in pup- induced maternal behavior. Moreover, primiparous heterozygous females exhibit a profound deficit in maternal care when challenged with foste r pups. Morris maze studies revealed normal configural learning in the heterozygous and homozygous animals. Eating, locomotor activity, sexu al behavior, and exploration tall processes regulated by the hypothala mus) are normal in PRLR mutant mice. Olfactory function was tested in an aversive conditioning paradigm, results indicating that heterozygou s and homozygous PRLR mutant mice are not anosmic. These studies clear ly establish the PRLR as a regulator of maternal behavior.