Central Gain Restores Auditory Processing following Near-Complete Cochlear Denervation.
Central Gain Restores Auditory Processing following Near-Complete Cochlear Denervation.
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DOI：
10.1016/j.neuron.2015.12.041
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发表时间：
2016-02-17
期刊：
影响因子：
16.2
通讯作者：
Polley DB
中科院分区：
文献类型：
--
作者：
Chambers AR;Resnik J;Yuan Y;Whitton JP;Edge AS;Liberman MC;Polley DB
感觉器官损伤引起外周和大脑中的大量细胞和生理变化。在这里，我们表明，听觉处理的某些方面恢复深刻的耳蜗去神经后，由于在更高阶段的中央听觉通路的渐进性，补偿可塑性。损伤>95%的耳蜗神经传入突触，同时保留毛细胞，在成年小鼠中几乎消除了听觉脑干反应和声学惊吓反射，但音调检测行为几乎正常。随着听觉神经的声音诱发反应在去神经支配后逐渐减弱，皮层（以及较小程度上的中脑）的声音诱发活动反弹或超过控制水平。增加的中央增益支持恢复基本的声音特征编码的放电率，但没有功能编码的精确尖峰定时，如调制噪声或语音。这些发现强调了中枢可塑性在耳蜗性听力障碍的感知后遗症中的重要性。
Sensory organ damage induces a host of cellular and physiological changes in the periphery and the brain. Here, we show that some aspects of auditory processing recover after profound cochlear denervation due to a progressive, compensatory plasticity at higher stages of the central auditory pathway. Lesioning >95% of cochlear nerve afferent synapses, while sparing hair cells, in adult mice virtually eliminated the auditory brainstem response and acoustic startle reflex, yet tone detection behavior was nearly normal. As sound-evoked responses from the auditory nerve grew progressively weaker following denervation, sound-evoked activity in the cortex – and to a lesser extent the midbrain – rebounded or surpassed control levels. Increased central gain supported the recovery of rudimentary sound features encoded by firing rate, but not features encoded by precise spike timing such as modulated noise or speech. These findings underscore the importance of central plasticity in the perceptual sequelae of cochlear hearing impairment.