Anti-Epileptic Drugs Delay Age-Related Loss of Spiral Ganglion Neurons via T-type Calcium Channel

Debin Lei; Xia Gao; Philip Perez; Kevin K Ohlemiller; Chien-Chang Chen; Kevin P Campbell; Aizhen Yang Hood; Jianxin Bao

doi:10.1016/j.heares.2011.05.010

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Anti-Epileptic Drugs Delay Age-Related Loss of Spiral Ganglion Neurons via T-type Calcium Channel

Journal article

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Anti-Epileptic Drugs Delay Age-Related Loss of Spiral Ganglion Neurons via T-type Calcium Channel

Debin Lei, Xia Gao, Philip Perez, Kevin K Ohlemiller, Chien-Chang Chen, Kevin P Campbell, Aizhen Yang Hood and Jianxin Bao

Hearing research, Vol.278(1-2), pp.106-112

08/2011

DOI: 10.1016/j.heares.2011.05.010

PMCID: PMC3152691

PMID: 21640179

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Abstract

Loss of spiral ganglion neurons is a major cause of age-related hearing loss (presbycusis). Despite being the third most prevalent condition afflicting elderly persons, there are no known medications to prevent presbycusis. Because calcium signaling has long been implicated in age-related neuronal death, we investigated T-type calcium channels. This family is comprised of three members (Ca v 3.1, Ca v 3.2, and Ca v 3.3), based on their respective main pore-forming alpha subunits: α1G, α1H, and α1I. In the present study, we report a significant delay of age-related loss of cochlear function and preservation of spiral ganglion neurons in α 1H null and heterozygous mice, clearly demonstrating an important role for Ca v 3.2 in age-related neuronal loss. Furthermore, we show that anticonvulsant drugs from a family of T-type calcium channel blockers can significantly preserve spiral ganglion neurons during aging. To our knowledge, this is the first report of drugs capable of diminishing age-related loss of spiral ganglion neurons.

Spiral ganglion neuron

Anti-epileptic drug

Aging

Hair cell

Presbycusis

Details

Title: Subtitle: Anti-Epileptic Drugs Delay Age-Related Loss of Spiral Ganglion Neurons via T-type Calcium Channel
Creators: Debin Lei - Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
Xia Gao - Department of Otolaryngology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China 210008
Philip Perez - Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
Kevin K Ohlemiller - Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
Chien-Chang Chen - Howard Hughes Medical Institute, University of Iowa, Iowa City, Iowa, 60153, USA
Kevin P Campbell - Howard Hughes Medical Institute, University of Iowa, Iowa City, Iowa, 60153, USA
Aizhen Yang Hood - Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
Jianxin Bao - Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
Resource Type: Journal article
Publication Details: Hearing research, Vol.278(1-2), pp.106-112
DOI: 10.1016/j.heares.2011.05.010
PMID: 21640179
PMCID: PMC3152691
NLM abbreviation: Hear Res
ISSN: 0378-5955
eISSN: 1878-5891
Grant note: R21 DC010489-01 || DC / National Institute on Deafness and Other Communication Disorders : NIDCD
Language: English
Date published: 08/2011
Academic Unit: Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute
Record Identifier: 9984020990002771

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