The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice
Abstract The mammalian cochlea possesses unique acoustic sensitivity due to a mechanoelectrical ‘amplifier’, which requires the metabolic support of the cochlear lateral wall. Loud sound exposure sufficient to induce permanent hearing damage causes cochlear blood flow reduction, which may contribute...
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Nature Portfolio
2020
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oai:doaj.org-article:778a5759aace478a88513290c49862352021-12-02T17:52:14ZThe mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice10.1038/s41598-020-66192-62045-2322https://doaj.org/article/778a5759aace478a88513290c49862352020-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-66192-6https://doaj.org/toc/2045-2322Abstract The mammalian cochlea possesses unique acoustic sensitivity due to a mechanoelectrical ‘amplifier’, which requires the metabolic support of the cochlear lateral wall. Loud sound exposure sufficient to induce permanent hearing damage causes cochlear blood flow reduction, which may contribute to hearing loss. However, sensory epithelium involvement in the cochlear blood flow regulation pathway is not fully described. We hypothesize that genetic manipulation of the mechanoelectrical transducer complex will abolish sound induced cochlear blood flow regulation. We used salsa mice, a Chd23 mutant with no mechanoelectrical transduction, and deafness before p56. Using optical coherence tomography angiography, we measured the cochlear blood flow of salsa and wild-type mice in response to loud sound (120 dB SPL, 30 minutes low-pass filtered noise). An expected sound induced decrease in cochlear blood flow occurred in CBA/CaJ mice, but surprisingly the same sound protocol induced cochlear blood flow increases in salsa mice. Blood flow did not change in the contralateral ear. Disruption of the sympathetic nervous system partially abolished the observed wild-type blood flow decrease but not the salsa increase. Therefore sympathetic activation contributes to sound induced reduction of cochlear blood flow. Additionally a local, non-sensory pathway, potentially therapeutically targetable, must exist for cochlear blood flow regulation.George W. S. BurwoodSuzan DziennisTeresa WilsonSarah FosterYuan ZhangGangjun LiuJianlong YangSean ElkinsAlfred L. NuttallNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-11 (2020) |
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DOAJ |
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DOAJ |
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EN |
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Medicine R Science Q |
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Medicine R Science Q George W. S. Burwood Suzan Dziennis Teresa Wilson Sarah Foster Yuan Zhang Gangjun Liu Jianlong Yang Sean Elkins Alfred L. Nuttall The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| description |
Abstract The mammalian cochlea possesses unique acoustic sensitivity due to a mechanoelectrical ‘amplifier’, which requires the metabolic support of the cochlear lateral wall. Loud sound exposure sufficient to induce permanent hearing damage causes cochlear blood flow reduction, which may contribute to hearing loss. However, sensory epithelium involvement in the cochlear blood flow regulation pathway is not fully described. We hypothesize that genetic manipulation of the mechanoelectrical transducer complex will abolish sound induced cochlear blood flow regulation. We used salsa mice, a Chd23 mutant with no mechanoelectrical transduction, and deafness before p56. Using optical coherence tomography angiography, we measured the cochlear blood flow of salsa and wild-type mice in response to loud sound (120 dB SPL, 30 minutes low-pass filtered noise). An expected sound induced decrease in cochlear blood flow occurred in CBA/CaJ mice, but surprisingly the same sound protocol induced cochlear blood flow increases in salsa mice. Blood flow did not change in the contralateral ear. Disruption of the sympathetic nervous system partially abolished the observed wild-type blood flow decrease but not the salsa increase. Therefore sympathetic activation contributes to sound induced reduction of cochlear blood flow. Additionally a local, non-sensory pathway, potentially therapeutically targetable, must exist for cochlear blood flow regulation. |
| format |
article |
| author |
George W. S. Burwood Suzan Dziennis Teresa Wilson Sarah Foster Yuan Zhang Gangjun Liu Jianlong Yang Sean Elkins Alfred L. Nuttall |
| author_facet |
George W. S. Burwood Suzan Dziennis Teresa Wilson Sarah Foster Yuan Zhang Gangjun Liu Jianlong Yang Sean Elkins Alfred L. Nuttall |
| author_sort |
George W. S. Burwood |
| title |
The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| title_short |
The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| title_full |
The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| title_fullStr |
The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| title_full_unstemmed |
The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| title_sort |
mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice |
| publisher |
Nature Portfolio |
| publishDate |
2020 |
| url |
https://doaj.org/article/778a5759aace478a88513290c4986235 |
| work_keys_str_mv |
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