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

Abstract

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.

SUPPLEMENTAL MATERIAL

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

ACKNOWLEDGMENTS

We thank Jeremy Smith, Matthew Cunningham, Stephanie Krasnow, and Heather Dungan for their critical review of earlier versions of this paper. We also thank Dawit Teklemichael and Blake Acohido for their invaluable help with establishment of the GALR2 KO colony at the University of Washington.

This work was supported by grants from the National Institutes of Health (R01 HD27142, SCCPRR U54 HD12629, R01 DK61517) and the National Science Foundation (IBN 0110686).