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The Journal of Neuroscience, February 1, 1999, 19(3):948-954

Functional Properties of Two Bombesin-Like Peptide Receptors Revealed by the Analysis of Mice Lacking Neuromedin B Receptor

Hiroko Ohki-Hamazaki^{1, 2}, Yasushi Sakai³, Katsuo Kamata⁴, Hiroo Ogura⁵, Shigeru Okuyama⁶, Kei Watase², Kazuyuki Yamada², and Keiji Wada²

¹ Department of Neurochemistry, Tokyo Institute of Psychiatry, Setagaya-ku, Tokyo 156-8585, Japan, ² Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan, ³ Laboratory of Physiology, Department of Occupational Therapy, College of Medical Sciences, Showa University, Midori-ku, Yokohama, Kanagawa 226-8555, Japan, ⁴ Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo 142-0063, Japan, ⁵ Tsukuba Research Laboratories, Eisai Company, Tsukuba, Ibaraki 300-2635, Japan, and ⁶ 1st Laboratory, Medicinal Research Laboratories, Taisho Pharmaceutical Company, Ohmiya, Saitama 330-8530, Japan

The neuromedin B-preferring receptor (NMB-R) is one of the members of the bombesin (BN)-like peptide receptor subfamily in mammals. Previously, we have generated and characterized mice with targeted disruption of the two other BN-like peptide receptors, bombesin receptor subtype-3 (BRS-3) and gastrin-releasing peptide-preferring receptor (GRP-R). Here we describe the generation and analysis of NMB-R-deficient mice to investigate how NMB-R differs from BRS-3 and GRP-R. Compensation for NMB-R deficiency by overexpression of GRP-R and/or BRS-3 was not detected. Although the hypothermic effect of NMB was reduced by 50% in NMB-R-deficient mice, the effect of GRP infusion was comparable to the wild-type mice. In contrast, fundic smooth muscle contraction on stimulation with NMB or GRP was normal in NMB-R-deficient mice. Administration of GRP but not NMB suppressed glucose intake in both normal and NMB-R-deficient mice. These results suggest that the NMB-R has an essential role in thermoregulation, but not for smooth muscle contraction of the fundus or for the suppression of feeding behavior. In addition, the behavioral phenotypes of GRP-R-deficient mice were not observed in NMB-R-deficient mice. These data show that the functions of NMB-R and GRP-R are distinct, with only partial overlap.

Key words: neuromedin B receptor; gastrin-releasing peptide receptor; smooth muscle contraction; thermoregulation; feeding suppression; social behavior; knock-out mice

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Copyright © 1999 Society for Neuroscience  0270-6474/99/193948-07$05.00/0

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