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J. Biol. Chem., Vol. 282, Issue 51, 37225-37231, December 21, 2007

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Abnormal Taste Perception in Mice Lacking the Type 3 Inositol 1,4,5-Trisphosphate Receptor^*

Chihiro Hisatsune¹, Keiko Yasumatsu^¶, Hiromi Takahashi-Iwanaga^||, Naoko Ogawa, Yukiko Kuroda, Ryusuke Yoshida^¶, Yuzo Ninomiya^¶, and Katsuhiko Mikoshiba^**2

From the Laboratory for Developmental Neurobiology, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako city, Saitama 351-0198, Japan, Division of Molecular Neurobiology, Institute of Medical Science, University of Tokyo, 3-4-1, Shirokane-dai, Minato-ku, Tokyo 108-8639, Japan, ^¶Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan, ^||Department of Anatomy, School of Medicine, Hokkaido University, Sapporo 060-8638, Japan, and ^**Calcium Oscillation Project, ICORP, Japan Science and Technology Agency, 3 Nibancho, Chiyoda-ku, Tokyo 102-0084, Japan

Inositol 1,4,5-trisphosphate receptor (IP₃R) is one of the important calcium channels expressed in the endoplasmic reticulum and has been shown to play crucial roles in various physiological phenomena. Type 3 IP₃R is expressed in taste cells, but the physiological relevance of this receptor in taste perception in vivo is still unknown. Here, we show that mice lacking IP₃R3 show abnormal behavioral and electrophysiological responses to sweet, umami, and bitter substances that trigger G-protein-coupled receptor activation. In contrast, responses to salty and acid tastes are largely normal in the mutant mice. We conclude that IP₃R3 is a principal mediator of sweet, bitter, and umami taste perception and would be a missing molecule linking phospholipase C β2 to TRPM5 activation.

Received for publication, July 10, 2007 , and in revised form, September 14, 2007.

^* This work was supported by grants from the Ministry of Education, Science, and Culture of Japan (to K. M. and Y. N.), a grant-in-aid for young scientists (to C. H.), and the Japan Science and Technology Agency. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1.

¹ To whom correspondence may be addressed: Tel.: 81-48-467-9745; Fax: 81-48-467-9744; E-mail: chihiro{at}brain.riken.go.jp.

² To whom correspondence may be addressed: E-mail: mikosiba{at}brain.riken.go.jp.

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