Chambers Anna R, Resnik Jennifer, Yuan Yasheng, Whitton Jonathon P, Edge Albert S, Liberman M Charles, Polley Daniel B
Eaton-Peabody Laboratories, Massachusetts Eye and Ear Infirmary, Boston, MA 02114, USA.
Eaton-Peabody Laboratories, Massachusetts Eye and Ear Infirmary, Boston, MA 02114, USA; Department of Otolaryngology, Harvard Medical School, Boston, MA 02114, USA.
Neuron. 2016 Feb 17;89(4):867-79. doi: 10.1016/j.neuron.2015.12.041. Epub 2016 Jan 28.
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.
感觉器官损伤会在周围和大脑中引发一系列细胞和生理变化。在此,我们表明,由于中枢听觉通路较高阶段存在渐进性的代偿性可塑性, profound cochlear denervation后听觉处理的某些方面得以恢复。在成年小鼠中,损伤超过95%的耳蜗神经传入突触,同时保留毛细胞,几乎消除了听觉脑干反应和听觉惊吓反射,但音调检测行为几乎正常。随着去神经支配后来自听觉神经的声音诱发反应逐渐减弱,皮层以及程度较轻的中脑中的声音诱发活动反弹或超过对照水平。增加的中枢增益支持了由放电率编码的基本声音特征的恢复,但不支持由精确的尖峰时间编码的特征,如调制噪声或语音。这些发现强调了中枢可塑性在耳蜗听力损伤感知后遗症中的重要性。