Changes in auditory brain stem responses and inner hair cell synapses after moderate noise exposures.

Abstract

Noise induced hearing loss is a major health problem worldwide (Sliwinska- Kowalska and Davis 2012). After noise exposure, hair cell damage is associated with reduced hearing sensitivity but increasing evidence shows that the neural injury, ranging from synaptic damage through to the loss of dendrites and spiral ganglion cells, has been underestimated (Kujawa and Liberman 2006). Recent studies have shown that rapid, extensive and irreversible loss of synapses occur within 24 hour post-exposure and delayed, progressive loss of cochlear neurons over several months, although hair cells remain and recover normal function. Despite the recovery of threshold sensitivity, the consequences of such primary neuronal loss on auditory processing of supra-thresholds sounds are likely difficult in noisy environment (Kujawa and Liberman 2009). Here, we examined the impact of noise on cochlear structure by closely examining the changes in auditory brainstem response (ABR) thresholds, amplitude of wave I of the ABR, which constitutes the activity of the primary auditory neuronsand the of IHC-type I SGN synapses. Thresholds were measured to determine noise exposure parameters that induced TTS in the experimental C57BL/6 mice. Noise exposures at 85dB or 90 dB (octave band pass 8- 16 kHz or 16- 24 kHz, 2 hr) were used and ABR thresholds and wave 1 amplitudes were measured pre-, 1 day and 1 week post noise exposure. It was shown that noise exposure (8 – 16 kHz) at 90 dB resulted in PTS whereas 85 dB produced TTS. However, unlike previous papers, changes in ABR wave I amplitude was not seen in mice with TTS. This was also reflected in the synapse counts. . This suggested that in C57BL/6 mice, noise exposure that induced TTS did not produce significant changes in auditory nerve function and IHC synapses. Noise exposures of 16 – 24 kHz either produced marginal TTS of 5dB, or a PTS at the higher frequencies. Our studies suggest that there is a narrow window between inducing TTS and PTS in C57BL/6 mice. There may be an interaction between the genes that produce an early onset age related hearing loss in these mice and the environment (noise) which produces this different susceptibility to noise in this mouse strain. This is important when considering the effect of noise induced hearing loss in human subjects.