Abstract
A robust temporary threshold shift (TTS) can create significant primary damage to the auditory synapse, termed cochlear synaptopathy (CS). The common model applied to examination of this pathology is a single noise exposure or extended duration exposures at relatively high noise dosages. It is unclear if a single noise exposure that does not produce physiological changes consistent with CS (such as suppressed suprathreshold responses) can create evidence consistent with the pathology induced by repeated exposures. Here, we exposed 16-week (wk) old Sprague-Dawley rats to repeated noise exposures (4 consecutive days, 8–16 kHz octave-band of noise, 97 dB SPL for 2 h) and examined measures of cochlear function (distortion product otoacoustic emissions) and auditory neural integrity (auditory brainstem response, wave 1 amplitude). Our results demonstrated a mean maximal threshold shift of 16 dB at 24 h post the initial noise exposure. Subsequent daily repeated exposures (4 consecutive days) resulted in diminished threshold shift at 24 h post repeated TTS. In addition to recovered thresholds, no sustained reduction in suprathreshold responses was observed. The findings are consistent with conditioning literature suggesting diminished TTS with repeated exposures. Repeated TTS that was not individually synaptopathic did not produce physiological evidence consistent with acute CS.
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