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. 2022 Feb 10;16:799787. doi: 10.3389/fnins.2022.799787

FIGURE 4.

FIGURE 4

Perceptual consequences of sensorineural hearing loss. (Ai,ii,iii) Diagram of cochlear hair cells and spiral ganglion neuron connectivity under normal (Ai) or pathological conditions of synaptopathy (Aii), or sensory hair cell damage (Aiii). (Ai) Purple: over 95% of afferent input to central auditory system comes from type 1 spiral ganglion neurons (SGN) that form synaptic contacts inner hair cells (IHCs), the main conventional sensory receptors of the cochlea. IHCs are innervated by multiple (10–20) type I neurons but each type I neuron only contacts a single IHC. Green: unmyelinated type II SGNs form synaptic contacts with multiple outer hair cells (OHCs) but each OHC only receives one contact from one Type-II neuron. Type-II SGNs represent only 5% of afferent input and are not involved with transmission of acoustic information to brain. Rather, the major role of OHCs is to amplify the cochlear mechanical response to low-level input, providing increased sensitivity to low intensity sounds. (Aii) In the synaptopathic ear, many of the synaptic contacts between type I SGNs and IHCs have degenerated, leaving fewer afferent nerve fibers to relay sound information from the ear to the brain, which may underly hidden hearing loss and impaired speech-in-noise perception. (Aiii) Many forms of acquired sensorineural hearing loss are associated with damage to OHCs and disruption to mechanical cochlear gain control mechanisms, leading to permanent threshold shifts, loudness recruitment, and broader frequency tuning. (B) Tone detection behavior in animals with selective damage the type I SGN-IHC complex (purple) is remarkably normal under quiet conditions, even with moderate to severe cochlear deafferentation. (C) Tone-in-noise detection is more severely impaired in animals with selective damage the type I SGN-IHC complex (purple) even though thresholds in quiet are maintained. Schematized data in panels (B,C) adapted from Resnik and Polley (2021). (D) Auditory reaction time (RT) measures of loudness growth in animal models (Radziwon and Salvi, 2020) have demonstrated that some forms of hearing loss can result in abnormal increases to the slope of RT-intensity functions, consistent with loudness recruitment and/or hyperacusis.