Seminars in Hearing Research at Purdue (SHRP)

Title:  Examining the Physiologic Phenotype of Cochlear Synaptopathy Using Narrowband Chirp-Evoked Compound Action Potentials

Speaker: Ivy Schweinzger, Ph.D. - Post-doctoral Research Associate (Bharwadwaj and Heinz labs), SLHS

Date: Dec 5, 2019
Time: 10:30 – 11:20 am
Location: LYLE 1150

Abstract:

Recent research in animals has found that following noise levels that induce a temporary threshold shift (TTS), there is permanent degeneration of ribbon synapses connecting auditory neurons to inner hair cells even though outer hair cell function has returned to normal. This leads to eventual degeneration of auditory nerve fibers (ANFs), specifically those of low-spontaneous rates (SR) and high-thresholds, which encode high-intensity sounds. This phenomenon has been termed cochlear synaptopathy.

The physiologic phenotype of cochlear synaptopathy presents as normal hair cell functioning and neural thresholds with degraded auditory nerve activity in response to high-intensity sounds, which is indicative of damage to low-SR ANFs. The purpose of this project was to expand on current animal research findings regarding noise-induced hearing impairment by comparing the auditory nerve activity evoked using a signal-in-noise action potentials (SiNAPs) technique to that evoked with both narrowband chirp and toneburst stimuli in quiet. Furthermore, using this technique, this study aimed to determine if music, a more human-typical exposure, produced the physiologic phenotype of cochlear synaptopathy when gerbils were exposed at levels deemed both safe and unsafe according to standards set for human hearing by the National Institute of Occupational Safety and Health (NIOSH).

Animals were separated into three groups: unexposed, a safe exposure group -exposed for 2 hours with a time-weighted average of 90 dBA -, and an unsafe exposure group – exposed for 2 hours with a time-weighted average of 100 dBA. Auditory brainstem responses (ABR) were measured pre-music exposure, immediately post-music exposure and two weeks post-music exposure. Compound action potential (CAP) responses were then recorded at the two-week post-exposure time point. Results showed that exposed animals had SiNAPs responses that were significantly degraded in amplitude as compared with SiNAPs responses for unexposed animals [F(9,1250)=188,p<.001]. The amplitude of responses shown with ABR amplitude-intensity functions did not significantly differ between the unexposed group and the safe and unsafe exposure groups at two weeks post-noise time points [F(2)=0.406, p=0.674]. However, there was a significant shift in ABR thresholds for both exposure groups immediately following the noise exposure. The recovery from TTS observed in ABR findings, coupled with the degraded auditory nerve responses to 2 kHz narrowband chirp SiNAPs at intense levels (i.e., 80 dB SPL) suggests damage to low-SR ANFs caused by the high-intensity music exposure.

Animals that were exposed to noise at safe levels showed similar auditory evoked potential amplitudes as did animals who were exposed at unsafe levels. These findings suggest that exposure to music at levels deemed “safe” can cause physiological changes at the auditory peripheral level that are suggestive of both cochlear synaptopathy and permanent anatomical damage to outer hair cells as well as nerve fibers in some frequency regions of the gerbil cochlea.  Moving forward, Mongolian gerbils may be an optimal translational model for research on noise-induced hearing loss given the similarity of the noise susceptible region with that of humans.

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