Effect of Unilateral Acoustic Trauma on Neuronal Firing Activity in the Inferior Colliculus of Mice.

Chun-Jen Hsiao,Alexander V Galazyuk

doi:10.3389/fnsyn.2021.684141

Chun-Jen Hsiao, Alexander V Galazyuk

Open Access

https://doi.org/10.3389/fnsyn.2021.684141

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Abstract

Neural hyperactivity induced by sound exposure often correlates with the development of hyperacusis and/or tinnitus. In laboratory animals, hyperactivity is typically induced by unilateral sound exposure to preserve one ear for further testing of hearing performance. Most ascending fibers in the auditory system cross into the superior olivary complex and then ascend contralaterally. Therefore, unilateral exposure should be expected to mostly affect the contralateral side above the auditory brain stem. On the other hand, it is well known that a significant number of neurons have crossing fibers at every level of the auditory pathway, which may spread the effect of unilateral exposure onto the ipsilateral side. Here we demonstrate that unilateral sound exposure causes development of hyperactivity in both the contra and ipsilateral inferior colliculus in mice. We found that both the spontaneous firing rate and bursting activity were increased significantly compared to unexposed mice. The neurons with characteristic frequencies at or above the center frequency of exposure showed the greatest increase. Surprisingly, this increase was more pronounced in the ipsilateral inferior colliculus. This study highlights the importance of considering both ipsi- and contralateral effects in future studies utilizing unilateral sound exposure.

Highlights

Neuronal hyperactivity is present in many brain diseases
To assess the effect of unilateral acoustic trauma on hearing, the Auditory Brainstem Responses (ABR) thresholds were determined in four mice before, directly following, and 1 month post-exposure in both ears
We found a temporary threshold increase at 12.5, 20, 30, and 40 kHz right after sound exposure in the exposed ear which recovered to control levels 1 month later (Figure 1A)

Summary

Introduction

Neuronal hyperactivity is present in many brain diseases. In the auditory system it is believed that hyperactivity may underlie both hyperacusis (exaggerated sensitivity to sound) and tinnitus (a phantom sound without an external stimulus) (Gerken, 1996; Salvi et al, 2000; Eggermont and Roberts, 2004; Roberts et al, 2010; Galazyuk et al, 2012; Salloum et al, 2016; Shore et al, 2016). It has been shown that sound exposure leads to cochlear damage and subsequent threshold shifts (Liberman and Kiang, 1978; Kujawa and Liberman, 2009). In response to this damage, the central auditory system increases its gain to compensate for the reduced sensorineural input from the cochlea (Salvi et al, 2000; Schaette and McAlpine, 2011; Galazyuk et al, 2012; Auerbach et al, 2014). As a result of this change in gain, hyperactivity develops in the auditory system as well as in non-auditory brain structures. Noise-induced hyperactivity has been described for the cochlear nucleus (Kaltenbach and Afman, 2000; Brozoski and Bauer, 2005), inferior colliculus (Ma et al, 2006; Bauer et al, 2008; Mulders and Robertson, 2013; Ropp et al, 2014), Hyperactivity in the Inferior Colliculus medial geniculate nucleus (Kalappa et al, 2014), and auditory cortex (Syka and Rybalko, 2000), but not necessarily in auditory nerve fibers (Eggermont and Roberts, 2004)

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