ATP-gated ion channels mediate adaptation to elevated sound levels

Housley G.D.; Morton-Jones R.; Vlajkovic S.M.Telang R.S.Paramananthasivam V.Tadros S.F.Wong A.Y.Froud K.E.Cederholm J.M.E.Sivakumaran Y.Snguanwongchai P.Khakh B.S.Cockayne D.A.Thorne P.R.Ryan A.F.

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ATP-gated ion channels mediate adaptation to elevated sound levels

机译：ATP-gated ion channels mediate adaptation to elevated sound levels

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The sense of hearing is remarkable for its auditory dynamic range, which spans more than 10~(12) in acoustic intensity. The mechanisms that enable the cochlea to transduce high sound levels without damage are of key interest, particularly with regard to the broad impact of industrial, military, and recreational auditory overstimulation on hearing disability. We show that ATP-gated ion channels assembled from P2X_2 receptor subunits in the cochlea are necessary for the development of temporary threshold shift (TTS), evident in auditory brainstem response recordings as sound levels rise. In mice null for the P2RX_2 gene (encoding the P2X_2 receptor subunit), sustained 85-dB noise failed to elicit the TTS that wild-type (WT) mice developed. ATP released from the tissues of the cochlear partition with elevation of sound levels likely activates the broadly distributed P2X _2 receptors on epithelial cells lining the endolymphatic compartment. This purinergic signaling is supported by significantly greater noise-induced suppression of distortion product otoacoustic emissions derived from outer hair cell transduction and decreased suprathreshold auditory brainstem response input/output gain in WT mice compared with P2RX_2-null mice. At higher sound levels (≥95 dB), additional processes dominated TTS, and P2RX_2-null mice were more vulnerable than WT mice to permanent hearing loss due to hair cell synapse disruption. P2RX_2-null mice lacked ATP-gated conductance across the cochlear partition, including loss of ATP-gated inward current in hair cells. These data indicate that a significant component of TTS represents P2X_2 receptor-dependent purinergic hearing adaptation that underpins the upper physiological range of hearing.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2013年第18期|7494-7499|共6页
作者
Housley G.D.; Morton-Jones R.; Vlajkovic S.M.Telang R.S.Paramananthasivam V.Tadros S.F.Wong A.Y.Froud K.E.Cederholm J.M.E.Sivakumaran Y.Snguanwongchai P.Khakh B.S.Cockayne D.A.Thorne P.R.Ryan A.F.;
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作者单位

Department of Physiology and Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia;

Department of Physiology, School of Medical Sciences, University of Auckland, Auckland 1142, New Zealand;

Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, United StatesBoston Scientific, San Jose, CA 95134, United StatesDepartment of Surgery, University of California at San Diego, San Diego, CA 92037, United States;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
Acoustic overstimulation; Auditory neurotransmission; Noise-induced hearing loss; Permanent threshold shift; Sound transduction;

ATP-gated ion channels mediate adaptation to elevated sound levels

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