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Publication : Null mutation of the prolactin receptor gene produces a defect in maternal behavior.

First Author  Lucas BK Year  1998
Journal  Endocrinology Volume  139
Issue  10 Pages  4102-7
PubMed ID  9751488 Mgi Jnum  J:83247
Mgi Id  MGI:2660564 Doi  10.1210/endo.139.10.6243
Citation  Lucas BK, et al. (1998) Null mutation of the prolactin receptor gene produces a defect in maternal behavior. Endocrinology 139(10):4102-7
abstractText  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 foster pups. Morris maze studies revealed normal configural learning in the heterozygous and homozygous animals. Eating, locomotor activity, sexual behavior, and exploration (all processes regulated by the hypothalamus) are normal in PRLR mutant mice. Olfactory function was tested in an aversive conditioning paradigm, results indicating that heterozygous and homozygous PRLR mutant mice are not anosmic. These studies clearly establish the PRLR as a regulator of maternal behavior.
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