TY - JOUR
T1 - Central Gain Restores Auditory Processing following Near-Complete Cochlear Denervation
AU - Chambers, Anna R.
AU - Resnik, Jennifer
AU - Yuan, Yasheng
AU - Whitton, Jonathon P.
AU - Edge, Albert S.
AU - Liberman, M. Charles
AU - Polley, Daniel B.
N1 - Funding Information:
We thank Mark Liu and Krupa Shukla for assisting with behavioral measurements, Leslie Liberman for preparing cochlear whole mount sections, and Ken Hancock for programming assistance. This work was supported by R01 DC009836 (D.B.P.), R01 DC007174 (A.S.E.), R01 DC 00188 (M.C.L.), P30 05209 (M.C.L.), a research grant from Autifony Therapeutics (D.B.P.), and the Lauer Tinnitus Research Center (M.C.L. and D.B.P.).
Funding Information:
We thank Mark Liu and Krupa Shukla for assisting with behavioral measurements, Leslie Liberman for preparing cochlear whole mount sections, and Ken Hancock for programming assistance. This work was supported by R01 DC009836 (D.B.P.), R01 DC007174 (A.S.E.), R01 DC 00188 (M.C.L.), P30 05209 (M.C.L.), a research grant from Autifony Therapeutics (D.B.P.), and the Lauer Tinnitus Research Center (M.C.L. and D.B.P.).
Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/2/17
Y1 - 2016/2/17
N2 - 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. Video Abstract: Removing 95% of cochlear afferent synapses eliminates sound-evoked brainstem responses and acoustic reflexes, yet sound detection remains normal. Chambers and colleagues describe a cortical amplifier that recovers sound feature representations supported by neural rate-coding, but not precise spike timing.
AB - 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. Video Abstract: Removing 95% of cochlear afferent synapses eliminates sound-evoked brainstem responses and acoustic reflexes, yet sound detection remains normal. Chambers and colleagues describe a cortical amplifier that recovers sound feature representations supported by neural rate-coding, but not precise spike timing.
UR - http://www.scopus.com/inward/record.url?scp=84958225154&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2015.12.041
DO - 10.1016/j.neuron.2015.12.041
M3 - Article
AN - SCOPUS:84958225154
SN - 0896-6273
VL - 89
SP - 867
EP - 879
JO - Neuron
JF - Neuron
IS - 4
ER -