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Molecular and Cellular Biology, September 2004, p. 8048-8054, Vol. 24, No. 18
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.18.8048-8054.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Heterotrimeric G Proteins of the G_q/11 Family Are Crucial for the Induction of Maternal Behavior in Mice

Nina Wettschureck,^1* Alexandra Moers,¹ Tuula Hamalainen,² Thomas Lemberger,³ Günther Schütz,³ and Stefan Offermanns¹

Institute of Pharmacology, University of Heidelberg,¹ Deutsches Krebsforschungszentrum, Heidelberg, Germany,³ Department of Physiology, University of Turku, Turku, Finland²

Received 23 March 2004/ Returned for modification 24 April 2004/ Accepted 17 June 2004

Heterotrimeric G proteins of the G_q/11 family transduce signals from a variety of neurotransmitter receptors and have therefore been implicated in several functions of the central nervous system. To investigate the potential role of G_q/11 signaling in behavior, we generated mice which lack the -subunits of the two main members of the G_q/11 family, G_q and G₁₁, selectively in the forebrain. We show here that forebrain G_q/11-deficient females do not display any maternal behavior such as nest building, pup retrieving, crouching, or nursing. However, olfaction, motor behavior and mammary gland function are normal in forebrain G_q/11-deficient females. We used c-fos immunohistochemistry to investigate pup-induced neuronal activation in different forebrain regions and found a significant reduction in the medial preoptic area, the bed nucleus of stria terminalis, and the lateral septum both in postpartum females and in virgin females after foster pup exposure. Pituitary function, especially prolactin release, was normal in forebrain G_q/11-deficient females, and activation of oxytocin receptor-positive neurons in the hypothalamus did not differ between genotypes. Our findings show that G_q/11 signaling is indispensable to the neuronal circuit that connects the perception of pup-related stimuli to the initiation of maternal behavior and that this defect cannot be attributed to either reduced systemic prolactin levels or impaired activation of oxytocin receptor-positive neurons of the hypothalamus.

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* Corresponding author. Mailing address: Department of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany. Phone: 49-6221-548255. Fax: 49-6221-548549. E-mail: Nina.Wettschureck{at}urz.uni-heidelberg.de.

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Molecular and Cellular Biology, September 2004, p. 8048-8054, Vol. 24, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.18.8048-8054.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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