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J. Biol. Chem., Vol. 278, Issue 48, 48321-48329, November 28, 2003

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Function of -Aminobutyric Acid Receptor/Channel ₁ Subunits In Spinal Cord^*

Wei Zheng, Wenrui Xie, Jianhua Zhang, Judith A. Strong, Ling Wang, Lei Yu, Ming Xu, and Luo Lu¶

From the Division of Molecular Medicine, Harbor-UCLA Medical Center, The David Geffen School of Medicine University of California Los Angeles, Torrance, California 90502 and the Department of Cell Biology, Neurobiology and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267

-Aminobutyric acid (GABA) receptor/channel ₁ subunits are important components in inhibitory pathways in the central nervous system. However, the precise locations and roles of these receptors in the central nervous system are unknown. We studied the expression localization of GABA receptor/channel ₁ subunit in mouse spinal cord and dorsal root ganglia (DRG). The immunohistochemistry results indicated that GABA receptor/channel ₁ subunits were expressed in mouse spinal cord superficial dorsal horn (lamina I and lamina II) and in DRG. To understand the functions of the GABA receptor/channel ₁ subunit in these crucial sites of sensory transmission in vivo, we generated GABA receptor/channel ₁ subunit mutant mice (rho1^-/-). GABA receptor/channel ₁ subunit expression in the rho1^-/- mice was eliminated completely, whereas the gross neuroanatomical structures of the rho1^-/- mice spinal cord and DRG were unchanged. Electrophysiological recording showed that GABA-mediated spinal cord response was altered in the rho1^-/- mice. A decreased threshold for mechanical pain in the rho1^-/- mice compared with control mice was observed with the von Frey filament test. These findings indicate that the GABA receptor/channel ₁ subunit plays an important role in modulating spinal cord pain transmission functions in vivo.

Received for publication, July 21, 2003 , and in revised form, September 9, 2003.

^* This work is supported in part by National Institutes of Health Grants EY11653 (to L. L.), DA09444 and DA13471 (to L. Y.), DA13786 and DA14644 (to M. X.) and DA11284 (to J. Z.) and an Epilepsy Foundation grant (to M. X.). 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.

^¶ To whom correspondence should be addressed: Div. of Molecular Medicine, Harbor-UCLA Medical Center, 1124 W. Carson St., C-2, Torrance, CA 90502. Tel.: 310-787-6853; Fax: 310-222-6820; E-mail: lluou{at}ucla.edu.

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