Abstract
Objectives:
To create a noise-induced hearing loss (NIHL) mouse model to examine its effect on neuronal cells in the cochlear nucleus (CN), superior olivary complex (SOC), and lateral lemniscus (LL).
Methods:
Three month old CBA male mice were exposed to 110-120dB noise over 6 hours. Auditory brainstem response (ABR) tested at 1-day, 1-week, 1-month, and 2-months after acoustic trauma (AT) confirmed profound hearing loss. Distortion product otoacoustic emission (DPOAE) remained present after AT. FluoroGold (FG) was injected through the right tympanic membrane for retrocochlear neuronal staining.
Results:
The average click ABR threshold shifts were 55dB, 55dB, 45dB, and 48dB after 1-day, 1-week, 1-month, and 2-months post-AT, respectively. The average tonal ABR threshold shifts from 8-28 kHz were 51dB, 50.5dB, 49.8dB, and 43.8dB after 1-day, 1-week, 1-month, and 2-months, respectively. DPOAE signals from 12-28 kHz were present at higher thresholds (14.3dB, 12.7dB, 13dB, and 17dB after 1-day, 1-week, 1-month, and 2-months, respectively) after the NIHL. The average neuronal cell counts in the CN, SOC, LL, and contralateral SOC in deafened mice were 1390 ± 404, 2083 ± 190, 104 ± 21, and 163 ± 27, respectively; compared to 1483 ± 190, 2807 ± 67, 112 ± 20, and 208 ± 23, respectively, in control mice. The SOC yielded the only statistically significant difference between the two groups (P < 0.05).
Conclusions:
A reliable NIHL mouse model has been established. At 2-months post-deafening, we found significant decrease in neuronal cells in the SOC. This model serves as a tool to further investigate protective pharmacotherapy against NIHL.