Neuroscience
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The occurrence of tinnitus is associated with hearing loss and neuroplastic changes in the brain, but disentangling correlation and causation has remained difficult in both human and animal studies. Here we use earplugs to cause a period of monaural deprivation to induce a temporary, fully reversible tinnitus sensation, to test whether differences in subcortical changes in neural response gain, as reflected through changes in acoustic reflex thresholds (ARTs), could explain the occurrence of tinnitus. Forty-four subjects with normal hearing wore an earplug in one ear for either 4 (n = 27) or 7 days (n = 17). ⋯ There were no significant differences between the groups with 4 and 7 days of auditory deprivation. Our results suggest that either the subcortical neurophysiological changes underlying the ART reductions might not be related to the occurrence of tinnitus, or that they might be a necessary component of the generation of tinnitus, but with additional changes at a higher level of auditory processing required to give rise to tinnitus. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.
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The acoustic middle-ear-muscle reflex (MEMR) has been suggested as a sensitive non-invasive measure of cochlear synaptopathy, the loss of synapses between inner hair cells and auditory nerve fibers. In the present study, clinical MEMR thresholds were measured for 1-, 2-, and 4-kHz tonal elicitors, using a procedure shown to produce thresholds with excellent reliability. MEMR thresholds of 19 participants with tinnitus and normal audiograms were compared to those of 19 age- and sex-matched controls. ⋯ MEMR thresholds were unrelated to either SPiN or noise exposure, despite a wide range in both measures. It is possible that thresholds measured using a clinical paradigm are less sensitive to synaptopathy than those obtained using more sophisticated measurement techniques; however, we had good sensitivity at the group level, and even trends in the hypothesized direction were not observed. To the extent that MEMR thresholds are sensitive to cochlear synaptopathy, the present results provide no evidence that tinnitus, SPiN, or noise exposure are related to synaptopathy in the population studied.
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The central gain model of hyperacusis proposes that loss of auditory input can result in maladaptive neuronal gain increases in the central auditory system, leading to the over-amplification of sound-evoked activity and excessive loudness perception. Despite the attractiveness of this model, and supporting evidence for it, a critical test of the central gain theory requires that changes in sound-evoked activity be explicitly linked to perceptual alterations of loudness. Here we combined an operant conditioning task that uses a subject's reaction time to auditory stimuli to produce reliable measures of loudness growth with chronic electrophysiological recordings from the auditory cortex and inferior colliculus of awake, behaviorally-phenotyped animals. ⋯ Salicylate induced parallel changes to loudness growth and evoked response-intensity functions consistent with temporary hearing loss and hyperacusis. Most importantly, we found that salicylate-mediated changes in loudness growth and sound-evoked activity were correlated within individual animals. These results provide strong support for the central gain model of hyperacusis and demonstrate the utility of using an experimental design that allows for within-subject comparison of behavioral and electrophysiological measures, thereby making inter-subject variability a strength rather than a limitation.
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Auditory nerve fibers (ANFs) convey acoustic information from the sensory cells to the brainstem using an elaborated neural code based on both spike timing and rate. As the stimulus tone frequency increases, time coding fades and ceases, resulting in high-frequency tone encoding that relies mostly on the spike discharge rate. Here, we recapitulated our recent single-unit data from gerbil's auditory nerve to highlight the most relevant mode of coding (spike timing versus spike rate) in tone-in-noise. ⋯ Based on these findings, we first discuss the ecological function of the ANF distribution according to their spontaneous discharge rate. Then, we point out the poor synchronization of the low-SR ANFs, accounting for the discrepancy between ANF number and the amplitude of the compound action potential of the of the auditory nerve. Finally, we proposed a new diagnostic tool to assess low-SR fibers, which does not rely on the onset response of the ANFs.
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Noise-induced hidden hearing loss (NIHHL) has attracted great attention in hearing research and clinical audiology since the discovery of significant noise-induced synaptic damage in the absence of permanent threshold shifts (PTS) in animal models. Although the extant evidence for this damage is based on animal models, NIHHL likely occurs in humans as well. This review focuses on three issues concerning NIHHL that are somewhat controversial: (1) whether disrupted synapses can be re-established; (2) whether synaptic damage and repair are responsible for the initial temporal threshold shifts (TTS) and subsequent recovery; and (3) the relationship between the synaptic damage and repair processes and neural coding deficits. We conclude that, after a single, brief noise exposure, (1) the damaged and the totally destroyed synapses can be partially repaired, but the repaired synapses are functionally abnormal; (2) While deficits are observed in some aspects of neural responses related to temporal and intensity coding in the auditory nerve, we did not find strong evidence for hypothesized coding-in-noise deficits; (3) the sensitivity and the usefulness of the envelope following responses to amplitude modulation signals in detecting cochlear synaptopathy is questionable.