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Abstract
Noise-induced cochlear synaptopathy has been studied for over 20 years with no known diagnosis for this disorder within the human population. This type of “hidden hearing loss” induces a loss of synapses in the inner ear but no change in audiometric thresholds. Recent studies have shown that by two months post synaptopathy-inducing noise exposure, the synapses can regenerate. Meanwhile, animal studies to date have focused primarily on peripheral hearing measures to diagnose ribbon synapse loss while suggesting spatial hearing deficits result from this disorder and don’t account for the possible regeneration of synapses. Here, we measure binaural hearing both physiologically and behaviorally in guinea pigs with noise-induced cochlear synaptopathy. Physiological measurements were extended out to 2 months post noise exposure to account for any deficit and subsequent recovery.
I used adult pigmented Guinea pigs to study the mechanisms leading to hearing deficits resulting from a 2-hour moderate noise. Recent studies have shown that ribbon synapses regenerate after noise exposure in the guinea pig, therefore we extended our timepoints to 2 months post noise for physiological testing to account for any possible regeneration. I measured distortion product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs) to assay peripheral hearing at 6 timepoints. For the first time in a model of cochlear synaptopathy, I tested spatial hearing ability through the prepulse inhibition (PPI) of the acoustic startle reflex. PPI was used to measure minimal audible angle (MAA) and hearing-in-noise ability, or spatial release from masking, as this task approximates the ‘cocktail party’ effect. Lastly, I performed cochlear histology to assess any synaptic loss and performed staining for hair cells and ribbon synapses including both pre and post synaptic components.
Our results show that while common audiological assessments show a temporary threshold loss, reduced evoked potential amplitudes indicative of synaptopathy and measurable binaural electrophysiological hearing deficits post moderate noise exposure, all measures recover at 2 months post exposure including binaural behavior. Suspected regeneration of synaptic ribbons occurred by 2 months post noise and cochlear histology revealed no synaptic loss 4 months post noise exposure. We show that the same noise exposure that caused synaptic loss in prior studies causes binaural processing deficits in the brainstem and that the regeneration of synapses corresponds with recovered binaural processing including behavior. Results suggest that functional recovery of ribbon synapses post a single moderate noise exposure is sufficient to restore binaural hearing abilities.
