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Articles, Systems/Circuits

Aging after Noise Exposure: Acceleration of Cochlear Synaptopathy in “Recovered” Ears

Katharine A. Fernandez, Penelope W.C. Jeffers, Kumud Lall, M. Charles Liberman and Sharon G. Kujawa
Journal of Neuroscience 13 May 2015, 35 (19) 7509-7520; DOI: https://doi.org/10.1523/JNEUROSCI.5138-14.2015
Katharine A. Fernandez
1Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02115, and
2Eaton-Peabody Laboratories and
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Penelope W.C. Jeffers
2Eaton-Peabody Laboratories and
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Kumud Lall
1Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02115, and
2Eaton-Peabody Laboratories and
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M. Charles Liberman
1Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02115, and
2Eaton-Peabody Laboratories and
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Sharon G. Kujawa
1Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02115, and
2Eaton-Peabody Laboratories and
3Department of Audiology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114
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Abstract

Cochlear synaptic loss, rather than hair cell death, is the earliest sign of damage in both noise- and age-related hearing impairment (Kujawa and Liberman, 2009; Sergeyenko et al., 2013). Here, we compare cochlear aging after two types of noise exposure: one producing permanent synaptic damage without hair cell loss and another producing neither synaptopathy nor hair cell loss. Adult mice were exposed (8–16 kHz, 100 or 91 dB SPL for 2 h) and then evaluated from 1 h to ∼20 months after exposure. Cochlear function was assessed via distortion product otoacoustic emissions and auditory brainstem responses (ABRs). Cochlear whole mounts and plastic sections were studied to quantify hair cells, cochlear neurons, and the synapses connecting them. The synaptopathic noise (100 dB) caused 35–50 dB threshold shifts at 24 h. By 2 weeks, thresholds had recovered, but synaptic counts and ABR amplitudes at high frequencies were reduced by up to ∼45%. As exposed animals aged, synaptopathy was exacerbated compared with controls and spread to lower frequencies. Proportional ganglion cell losses followed. Threshold shifts first appeared >1 year after exposure and, by ∼20 months, were up to 18 dB greater in the synaptopathic noise group. Outer hair cell losses were exacerbated in the same time frame (∼10% at 32 kHz). In contrast, the 91 dB exposure, producing transient threshold shift without acute synaptopathy, showed no acceleration of synaptic loss or cochlear dysfunction as animals aged, at least to ∼1 year after exposure. Therefore, interactions between noise and aging may require an acute synaptopathy, but a single synaptopathic exposure can accelerate cochlear aging.

  • age-related hearing loss
  • auditory nerve
  • cochlear neuropathy
  • cochlear synaptopathy
  • noise-induced hearing loss
  • temporary threshold shift
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The Journal of Neuroscience: 35 (19)
Journal of Neuroscience
Vol. 35, Issue 19
13 May 2015
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Aging after Noise Exposure: Acceleration of Cochlear Synaptopathy in “Recovered” Ears
Katharine A. Fernandez, Penelope W.C. Jeffers, Kumud Lall, M. Charles Liberman, Sharon G. Kujawa
Journal of Neuroscience 13 May 2015, 35 (19) 7509-7520; DOI: 10.1523/JNEUROSCI.5138-14.2015

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Aging after Noise Exposure: Acceleration of Cochlear Synaptopathy in “Recovered” Ears
Katharine A. Fernandez, Penelope W.C. Jeffers, Kumud Lall, M. Charles Liberman, Sharon G. Kujawa
Journal of Neuroscience 13 May 2015, 35 (19) 7509-7520; DOI: 10.1523/JNEUROSCI.5138-14.2015
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Keywords

  • age-related hearing loss
  • auditory nerve
  • cochlear neuropathy
  • cochlear synaptopathy
  • noise-induced hearing loss
  • temporary threshold shift

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