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Molecular and Cellular Biology, June 2005, p. 4804-4811, Vol. 25, No. 11
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.11.4804-4811.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Phenotypic Analysis of Mice Deficient in the Type 2 Galanin Receptor (GALR2)

Michelle L. Gottsch,¹ Hongkui Zeng,² John G. Hohmann,² David Weinshenker,³ Donald K Clifton,⁴ and Robert A. Steiner^1,4,5*

Departments of Physiology & Biophysics,¹ Obstetrics & Gynecology,⁴ Biology, University of Washington, Seattle, Washington 98195-7290,⁵ Nura, Inc., Seattle, Washington,² Department of Human Genetics, Emory University, School of Medicine, Atlanta, Georgia³

Received 8 December 2004/ Returned for modification 4 February 2005/ Accepted 26 February 2005

Galanin is a neuropeptide implicated in the regulation of feeding, reproduction, cognition, nociception, and seizure susceptibility. There are three known galanin receptor (GALR) subtypes (GALR1, GALR2, and GALR3), which bind to galanin with different affinities and have their own unique distributions, signaling mechanisms, and putative functions in the brain and peripheral nervous system. To gain further insight into the possible physiological significance of GALR2, we created mutant mice that were deficient in GALR2 and compared their phenotype to that of wild-type (WT) littermate or age-matched controls, with respect to basic motor and sensory function, feeding behavior, reproduction, mood, learning and memory, and seizure susceptibility. Phenotypic analysis revealed that animals bearing a deletion of GALR2 did not differ significantly from their WT controls in any of the measured variables. We conclude that either GALR2 plays no role in these physiological functions or through redundancy or compensation these mutant animals can adapt to the congenital absence of GALR2. It is also conceivable that GALR2 plays only a subtle role in some of these functions and that the impact of its loss could not be detected by the analytical procedures used here.

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* Corresponding author. Mailing address: Department of Physiology & Biophysics, Health Sciences Building (G-424), School of Medicine, University of Washington, Box 357290, 1959 NE Pacific Street, Seattle, WA 98195-7290. Phone: (206) 543-8712. Fax: (206) 685-0619. E-mail: steiner{at}u.washington.edu.

Supplemental material for this article may be found at http://mcb.asm.org/.

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Molecular and Cellular Biology, June 2005, p. 4804-4811, Vol. 25, No. 11
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.11.4804-4811.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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