Details

Autor(en) / Beteiligte

• Altschuler, Richard A
• Stewart, Courtney E.
• Kabara, Lisa
• Martin, Catherine A.
• Kanicki, Ariane
• Kohrman, David C.
• Dolan, David F.

Titel

Noise overstimulation of young adult UMHET4 mice accelerates age-related hearing loss

Ist Teil von

• Hearing research, 2022-10, Vol.424, p.108601-108601, Article 108601

Ort / Verlag

Elsevier B.V

Erscheinungsjahr

2022

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• •A single exposure to noise given to young mice that does not cause immediate permanent hearing loss will accelerate and enhance later age-related hearing loss.•The effects of noise in youth on age-related hearing loss is largely an acceleration, with age-related hearing appearing earlier.•Different noise exposure conditions cause different paces and patterns of accelerated age-related hearing loss. Many factors contribute to hearing loss commonly found in older adults. There can be natural aging of cellular elements, hearing loss previously induced by environmental factors such as noise or ototoxic drugs as well as genetic and epigenetic influences. Even when noise overstimulation does not immediately cause permanent hearing loss it has recently been shown to increase later age-related hearing loss (ARHL). The present study further investigated this condition in the UMHET4 mouse model by comparing a small arms fire (SAF)-like impulse noise exposure that has the greatest immediate effect in more apical cochlear regions to a broadband noise (BBN) exposure that has the greatest immediate effect in more basal cochlear regions. Both noise exposures were given at levels that only induced temporary auditory brainstem response (ABR) threshold shifts (TS). Mice were noise exposed at 5 months of age followed by ABR assessment at 6, 12, 18, 21, and 24 months of age. Mice that received the SAF-like impulse noise had accelerated age-related TS at 4 kHz that appeared at 12 months of age (significantly increased compared to no-noise controls). This increased TS at 4 kHz continued at 18 and 21 months but was no longer significantly greater at 24 months of age. The SAF-like impulse noise also induced a significantly greater mean TS at 48 kHz, first appearing at 18 months of age and continuing to be significantly greater than controls at 21 and 24 months. The BBN induced a different pace and pattern of enhanced age-related ABR TS. The mean TS for the BBN group first became significantly greater than controls at 18 months of age and only at 48 kHz. It remained significantly greater than controls at 21 months but was no longer significantly greater at 24 months of age. Results, therefore, show different influences on ARHL for the two different noise exposure conditions. Noise-induced enhancement appears to provide more an acceleration than overall total increase in ARHL.