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Molecular and Cellular Biology, June 2007, p. 4500-4512, Vol. 27, No. 12
0270-7306/07/$08.00+0     doi:10.1128/MCB.02051-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Orphan Glutamate Receptor {delta}1 Subunit Required for High-Frequency Hearing{triangledown}

Jiangang Gao,1,{dagger} Stéphane F. Maison,2,{dagger} Xudong Wu,1 Keiko Hirose,3 Sherri M. Jones,4 Ildar Bayazitov,1 Yong Tian,1 Guy Mittleman,5 Douglas B. Matthews,5 Stanislav S. Zakharenko,1 M. Charles Liberman,2 and Jian Zuo1*

Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee,1 Department of Otology and Laryngology, Harvard Medical School and Eaton-Peabody Laboratory, Massachusetts Eye & Ear Infirmary, Boston, Massachusetts,2 Department of Otolaryngology, Cleveland Clinics Foundation, Cleveland, Ohio,3 Department of Communication Sciences and Disorders, East Carolina University, Greenville, North Carolina,4 Department of Psychology, University of Memphis, Memphis, Tennessee5

Received 2 November 2006/ Returned for modification 29 November 2006/ Accepted 6 April 2007

The function of the orphan glutamate receptor delta subunits (GluR{delta}1 and GluR{delta}2) remains unclear. GluR{delta}2 is expressed exclusively in the Purkinje cells of the cerebellum, and GluR{delta}1 is prominently expressed in inner ear hair cells and neurons of the hippocampus. We found that mice lacking the GluR{delta}1 protein displayed significant cochlear threshold shifts for frequencies of >16 kHz. These deficits correlated with a substantial loss of type IV spiral ligament fibrocytes and a significant reduction of endolymphatic potential in high-frequency cochlear regions. Vulnerability to acoustic injury was significantly enhanced; however, the efferent innervation of hair cells and the classic efferent inhibition of outer hair cells were unaffected. Hippocampal and vestibular morphology and function were normal. Our findings show that the orphan GluR{delta}1 plays an essential role in high-frequency hearing and ionic homeostasis in the basal cochlea, and the locus encoding GluR{delta}1 represents a candidate gene for congenital or acquired high-frequency hearing loss in humans.

* Corresponding author. Mailing address: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105. Phone: (901) 495-3891. Fax: (901) 495-2270. E-mail: jian.zuo{at}stjude.org

{triangledown} Published ahead of print on 16 April 2007.

{dagger} These authors contributed equally to this work.

Molecular and Cellular Biology, June 2007, p. 4500-4512, Vol. 27, No. 12
0270-7306/07/$08.00+0     doi:10.1128/MCB.02051-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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