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II型螺旋神经节传入神经元驱动内侧橄榄耳蜗反射对耳蜗放大器的抑制。

Type II spiral ganglion afferent neurons drive medial olivocochlear reflex suppression of the cochlear amplifier.

作者信息

Froud Kristina E, Wong Ann Chi Yan, Cederholm Jennie M E, Klugmann Matthias, Sandow Shaun L, Julien Jean-Pierre, Ryan Allen F, Housley Gary D

机构信息

Translational Neuroscience Facility and Department of Physiology, School of Medical Sciences, UNSW Australia, Sydney, New South Wales 2052, Australia.

1] Translational Neuroscience Facility and Department of Physiology, School of Medical Sciences, UNSW Australia, Sydney, New South Wales 2052, Australia [2] Departments of Surgery and Neurosciences, University of California San Diego, and Veterans Administration Medical Center, La Jolla, California 92093-0666, USA.

出版信息

Nat Commun. 2015 May 12;6:7115. doi: 10.1038/ncomms8115.

DOI:10.1038/ncomms8115
PMID:25965946
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4432632/
Abstract

The dynamic adjustment of hearing sensitivity and frequency selectivity is mediated by the medial olivocochlear efferent reflex, which suppresses the gain of the 'cochlear amplifier' in each ear. Such efferent feedback is important for promoting discrimination of sounds in background noise, sound localization and protecting the cochleae from acoustic overstimulation. However, the sensory driver for the olivocochlear reflex is unknown. Here, we resolve this longstanding question using a mouse model null for the gene encoding the type III intermediate filament peripherin (Prph). Prph((-/-)) mice lacked type II spiral ganglion neuron innervation of the outer hair cells, whereas innervation of the inner hair cells by type I spiral ganglion neurons was normal. Compared with Prph((+/+)) controls, both contralateral and ipsilateral olivocochlear efferent-mediated suppression of the cochlear amplifier were absent in Prph((-/-)) mice, demonstrating that outer hair cells and their type II afferents constitute the sensory drive for the olivocochlear efferent reflex.

摘要

听觉敏感性和频率选择性的动态调节是由内侧橄榄耳蜗传出反射介导的,该反射抑制每只耳朵中“耳蜗放大器”的增益。这种传出反馈对于促进在背景噪声中辨别声音、声音定位以及保护耳蜗免受声学过度刺激很重要。然而,橄榄耳蜗反射的感觉驱动因素尚不清楚。在这里,我们使用一种针对编码III型中间丝外周蛋白(Prph)的基因缺失的小鼠模型解决了这个长期存在的问题。Prph(-/-)小鼠缺乏外毛细胞的II型螺旋神经节神经元支配,而I型螺旋神经节神经元对内毛细胞的支配是正常的。与Prph(+/+)对照相比,Prph(-/-)小鼠中对耳蜗放大器的对侧和同侧橄榄耳蜗传出介导的抑制均不存在,这表明外毛细胞及其II型传入神经构成了橄榄耳蜗传出反射的感觉驱动。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/011a32be33e3/ncomms8115-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/c867c797fd8e/ncomms8115-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/b8ea9bc04947/ncomms8115-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/ca741bde9d69/ncomms8115-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/515ec0286775/ncomms8115-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/011a32be33e3/ncomms8115-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/c867c797fd8e/ncomms8115-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/b8ea9bc04947/ncomms8115-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/ca741bde9d69/ncomms8115-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/515ec0286775/ncomms8115-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b706/4432632/011a32be33e3/ncomms8115-f5.jpg

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