Early Loss of Spiral Ganglion Neurons in the Auditory System after Noise Trauma.

INTRODUCTION: Noise-induced hearing loss is one of the most frequent recognized occupational diseases. The time course of the involved pathologies is still under investigation. Several studies have demonstrated an acute damage of the sensory tissue, but only few experiments investigated the degeneration of (type I) spiral ganglion neurons (SGNs), representing the primary neurons in the auditory system. The aim of the present study was to investigate the time course of SGN degeneration within a 7-day period after traumatic noise exposure starting immediately after trauma. METHODS: Young adult normal hearing mice were noise exposed for 3 h with a broadband noise (5-20 kHz) at 115 dB SPL. Auditory threshold shift was measured by auditory brainstem recordings, and SGN densities were analyzed at different time points during the first week after acoustic trauma. RESULTS: Significant reduction of SGN densities was detected and is accompanied by a significant hearing loss. Degeneration starts within hours after the applied trauma, further progressing within days post-exposure. DISCUSSION: Early neurodegeneration in the auditory periphery seems to be induced by direct overstimulation of the auditory nerve fibers. SGN loss is supposed to be a result of inflammatory responses and neural deprivation, leading to permanent hearing loss and auditory processing deficits.

Neurodegeneration after repeated noise trauma in the mouse lower auditory pathway.

High intensity noise exposure leads to a permanent shift in auditory thresholds (PTS), affecting both peripheral (cochlear) tissue and the central auditory system. Studies have shown that a noise-induced hearing loss results in significant cell loss in several auditory structures. Degeneration can be demonstrated within hours after noise exposure, particularly in the lower auditory pathway, and continues to progress over days and weeks following the trauma. However, there is limited knowledge about the effects of recurring acoustic trauma. Repeated noise exposure has been demonstrated to increase neuroplasticity and neural activity. Thus, the present study aimed to investigate the influence of a second noise exposure on the cytoarchitecture of key structures of the auditory pathway, including spiral ganglion neurons (SGN), the ventral and dorsal cochlear nucleus (VCN and DCN, respectively), and the inferior colliculus (IC). In the experiments, young adult normal hearing mice were exposed to noise once or twice (with the second trauma applied one week after the initial exposure) for 3 h, using broadband white noise (5 - 20 kHz) at 115 dB SPL. The cell densities in the investigated auditory structures significantly decreased in response to the initial noise exposure compared to unexposed control animals. These findings are consistent with earlier research, which demonstrated degeneration in the auditory pathway within the first week after acoustic trauma. Additionally, cell densities were significantly decreased after the second trauma, but this effect was only observed in the VCN, with no similar effects seen in the SGN, DCN, or IC. These results illustrate how repeated noise exposure influences the cytoarchitecture of the auditory system. It appears that an initial noise exposure primarily damages the lower auditory pathway, but surviving cellular structures may develop resistance to additional noise-induced injury.