NYMC Faculty Publications

Dexamethasone's Effect in the Retrocochlear Auditory Centers of a Noise-Induced Hearing Loss Mouse Model

Author Type(s)

Faculty

DOI

10.1177/0194599814545771

Journal Title

Otolaryngology and Head and Neck Surgery

First Page

667

Last Page

674

Document Type

Article

Publication Date

10-1-2014

Department

Medicine

Keywords

Animals, Cochlear Nucleus, Dexamethasone, Disease Models, Animal, Evoked Potentials, Auditory, Brain Stem, Glucocorticoids, Hair Cells, Auditory, Hearing Loss, Noise-Induced, Male, Mice, Mice, Inbred CBA, Otoacoustic Emissions, Spontaneous, Superior Olivary Complex

Disciplines

Medicine and Health Sciences

Abstract

OBJECTIVE: Examine prophylactic effects of dexamethasone (Dex) in retrocochlear auditory centers in a noise-induced hearing loss (NIHL) mouse model.

STUDY DESIGN: Prospective animal study.

SETTING: Academic research center.

SUBJECTS AND METHODS: Thirty-two mice were divided into control, untreated, saline (2 and 10 µL), and Dex (2 and 10 µL) groups. Dex was applied intratympanically (IT) prior to 110 to 120 dB noise over 6 hours. Auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) were performed at 1 day, 1 week, 1 month, and 2 months. Retrocochlear neuronal cells were labeled with FluoroGold and counted. Hair cells of the organ of Corti were labeled with fluorescein isothiocyanate-conjugated phalloidin and counted.

RESULTS: Auditory brainstem response thresholds of untreated NIHL, 2 and 10 µL IT saline, and 2 and 10 µL IT Dex were 21.7 ± 2.9 dB, 20 ± 0 dB, 20 ± 5 dB, 18.3 ± 2.9 dB, and 18.3 ± 2.9 dB, respectively. At 1-day post NIHL, all groups demonstrated profound hearing loss. At 2 weeks, 2 and 10 µL Dex thresholds improved to 47.5 ± 3.5 dB and 48.8 ± 18.9 dB, respectively, whereas the untreated and saline groups remained unchanged. Mean cell counts in the cochlear nucleus (CN), superior olivary complex (SOC), and lateral lemniscus (LL) of control mice were 1483 ± 190, 2807 ± 67, and 112 ± 20, respectively. After acoustic trauma, the untreated, saline, and 2 µL Dex groups yielded decreased neuronal counts in the SOC. In contrast, the 10 µL Dex group had 1883 ± 186 (CN), 2774 ± 182 (SOC), and 166 ± 18 (LL). There was sporadic hair cell loss for all traumatized groups.

CONCLUSION: Our NIHL mouse model demonstrated dose-dependent Dex pretreatment otoprotection against NIHL with preservation of retrocochlear auditory neurons.

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