Normal aging results in a progressive loss of synapses between inner hair cells and auditory nerve fibers. An early overexposure to sound exacerbates this loss, even when thresholds recover. The functional consequences of this synaptopathy are poorly understood, though it is thought to affect suprathreshold coding of sound, especially in challenging listening conditions like the presence of background noise. Here, population level auditory brainstem responses (ABRs) and envelope following responses (EFRs) were used to study suprathreshold temporal processing with aging after an early noise exposure in a rodent model of synaptopathy.
ABRs and EFRs were obtained from an age-graded series of CBA/CaJ mice with or without a single exposure to a known synaptopathic noise that does not cause permanent hearing threshold elevations. ABRs were obtained to tone pips at various sound levels and frequencies. EFR stimuli were sinusoidally amplitude modulated
(sAM) tones. Stimuli were centred on synaptopathic or non-synaptopathic cochlear regions. The modulation frequency, depth, sound levels and signal-to-noise ratio
of the sAM stimuli were systematically varied to test temporal processing with degraded envelope cues. DPOAE thresholds and growth functions provided information about outer hair cell (OHC) functional integrity, and immunostained cochlear whole-mounts were used to quantify hair cells and synapses.
ABR wave 1 and EFRs measured from early neural sources both show progressive loss of amplitudes with age. Prior exposure to TTS-producing noise exaggerated these ongoing declines: As animals aged after noise, amplitude declines for both metrics exceeded those of age-matched controls in frequency regions of largest noise-induced synaptopathy. Pre-neural responses (DPOAEs, EFRs from pre-neural sources) were minimally affected until advanced age, when hair cell losses occur. Synaptopathic animals also showed a reduced dynamic range of encoding AM depth and noise masking in EFRs. These changes were present even though ABR and DPOAE thresholds and DPOAE amplitudes were similar to age-matched controls. Together, these changes are consistent with decreased temporal processing, exaggerated in the previously noise-exposed ears.
Age-related cochlear synaptopathy is accompanied by deficits in temporal processing at the earliest neural generators, resulting in a decrease in the dynamic range of encoding degraded envelope cues. These deficits are accelerated, but not fundamentally altered by an early over-exposure to noise. These results suggest that even a single exposure to synaptopathic noise can result in increased deficits in temporal processing throughout the lifespan.
DoD W81XWH-15-1-0103 (SGK)
|Period||13 Feb 2018|
|Event title||41st Midwinter Meeting of the Association for Research in Otolaryngology : null|
|Location||San Diego, United States, California|
|Degree of Recognition||International|
- cochlear synaptopathy