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Neurobiol Aging. 2016 Aug;44:173-184. doi: 10.1016/j.neurobiolaging.2016.05.001. Epub 2016 May 10.

Loss of auditory sensitivity from inner hair cell synaptopathy can be centrally compensated in the young but not old brain.

Author information

1
Department of Otolaryngology, Head & Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, University of Tübingen, Tübingen, Germany.
2
Department of Otolaryngology, Head & Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, University of Tübingen, Tübingen, Germany; Department of Otolaryngology, Head & Neck Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
3
Department of Otolaryngology, Head & Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, University of Tübingen, Tübingen, Germany. Electronic address: lukas.ruettiger@uni-tuebingen.de.

Abstract

A dramatic shift in societal demographics will lead to rapid growth in the number of older people with hearing deficits. Poorer performance in suprathreshold speech understanding and temporal processing with age has been previously linked with progressing inner hair cell (IHC) synaptopathy that precedes age-dependent elevation of auditory thresholds. We compared central sound responsiveness after acoustic trauma in young, middle-aged, and older rats. We demonstrate that IHC synaptopathy progresses from middle age onward and hearing threshold becomes elevated from old age onward. Interestingly, middle-aged animals could centrally compensate for the loss of auditory fiber activity through an increase in late auditory brainstem responses (late auditory brainstem response wave) linked to shortening of central response latencies. In contrast, old animals failed to restore central responsiveness, which correlated with reduced temporal resolution in responding to amplitude changes. These findings may suggest that cochlear IHC synaptopathy with age does not necessarily induce temporal auditory coding deficits, as long as the capacity to generate neuronal gain maintains normal sound-induced central amplitudes.

KEYWORDS:

Age-related hearing loss; Central compensation; Inner hair cell synaptopathy; Presbycusis

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