Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits.

Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Research Abstract Details 

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Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Abstract Text:

Sonja J Pyott,Andrea L Meredith,Anthony A Fodor,Ana E ,Ebenezer N Yamoah,Richard W Aldrich,

Large conductance voltage- and calcium-activated potassium (BK) channels are important for regulating many essential cellular functions, from neuronal action potential shape and firing rate to smooth muscle contractility. In amphibians, reptiles, and birds, BK channels mediate the intrinsic frequency tuning of the cochlear hair cell by an electrical resonance mechanism. In contrast, inner hair cells of the mammalian cochlea are extrinsically tuned by accessory structures of the cochlea. Nevertheless, BK channels are present in inner hair cells and encode a fast activating outward current. To understand the role of the BK channel alpha and beta subunits in mammalian inner hair cells, we analyzed the morphology, physiology, and function of these cells from mice lacking the BK channel alpha (Slo-/-) and also the beta1 and beta4 subunits (beta1/4-/-). Beta1/4-/- mice showed normal subcellular localization, developmental acquisition, and expression of BK channels. Beta1/4-/- mice showed normal cochlear function as indicated by normal auditory brainstem responses and distortion product otoacoustic emissions. Slo-/- mice also showed normal cochlear function despite the absence of the BKalpha subunit and the absence of fast activating outward current from the inner hair cells. Moreover, microarray analyses revealed no compensatory changes in transcripts encoding ion channels or transporters in the cochlea from Slo-/- mice. Slo-/- mice did, however, show increased resistance to noise-induced hearing loss. These findings reveal the fundamentally different contribution of BK channels to nonmammalian and mammalian hearing and suggest that BK channels should be considered a target in the prevention of noise-induced hearing loss.

Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Publishing Authors By Initials

SJ Pyott,AL Meredith,AA Fodor,AE ,EN Yamoah,RW Aldrich,

For similar proteins: protein subunits research abstracts see: proteins: protein subunits research

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Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 3312-24

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 29

MONTH: 11

YEAR: 2006

Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Keywords Mesh Terms:

KEYWORDS: Protein Subunits

MESH TERMS: genetics

Chemical & Substance for Abstract: Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. Information

Substance Name: Protein Subunits

Registry Number: 0

Grant and Affiliation Information for Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits.

AFFILIATION: Department of Otolaryngology Head and Neck Surgery, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA. spyott@jhmi.edu

Country: United States

AGENCY: United States NIDCD

GRANT: DC07592

ACRONYM: DC

MEDLINETA: J Biol Chem

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