Neuroscience
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The central auditory system shows a remarkable ability to rescale its neural representation of loudness following long-term, low-level acoustic exposures; even when the noise is presented intermittently. Circadian rhythms exert potent biological effects, but it remains unclear if acoustic exposures occurring during the light or dark cycle affect the neurophysiological changes involved in loudness rescaling. ⋯ However, neural activity in the inferior colliculus demonstrated negative gain in a frequency- and intensity-specific manner compared to unexposed controls; the magnitude and direction of the neuroplastic changes in the inferior colliculus were largely the same regardless of whether the 12-h noise exposures occurred during the light or dark phase of the circadian cycle. These neuroplastic changes could become relevant for low-level sound therapies used to treat hyperacusis.
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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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A noise-induced loss of inner hair cell (IHC) - auditory nerve synaptic connections has been suggested as a factor that can trigger the progression of maladaptive plastic changes leading to noise-induced tinnitus. The present study used a military relevant small arms fire (SAF)-like noise (50 biphasic impulses over 2.5 min at 152 dB SPL given unilaterally to the right ear) to induce loss (∼1/3) of IHC synaptic ribbons (associated with synapse loss) in rat cochleae with only minor (less than 10%) loss of outer hair cells. Approximately half of the noise-exposed rats showed poorer Gap Detection post-noise, a behavioral indication suggesting the presence of tinnitus. ⋯ The present study examined if this treatment would also reduce ribbon loss from the SAF-like noise exposure and if this would prevent the reduced Gap Detection. As in the previous study, piribedil, memantine, and ACEMg treatment significantly reduced the noise-induced loss of ribbons, such that it was no longer significantly different from normal. However, it did not prevent development of the reduced Gap Detection indication of tinnitus in all treated noise-exposed rats, reducing the incidence but not reaching significance.
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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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Many, or most, tinnitus models rely on increased central gain in the auditory pathway as all or part of the explanation, in that central auditory neurones deprived of their usual sensory input maintain homeostasis by increasing the rate at which they fire in response to any given strength of input, including amplifying spontaneous firing which forms the basis of tinnitus. However, dramatic gain changes occur in response to damage to the auditory periphery, irrespective of whether tinnitus occurs. This article considers gain in its broadest sense, summarizes its contributory processes, neural manifestations, behavioral effects, techniques for its measurement, pitfalls in attributing gain changes to tinnitus, a discussion of the minimum evidential requirements to implicate gain as a necessary and/or sufficient basis to explain tinnitus, and the extent of existing evidence in this regard. ⋯ A few studies show changes specifically attributable to tinnitus at group level, but the limited attempts so far to classify individual subjects based on gain metrics have not proven successful. If gain turns out to be unnecessary or insufficient to cause tinnitus, candidate additional mechanisms include focused attention, resetting of sensory predictions, failure of sensory gating, altered sensory predictions, formation of pervasive memory traces and/or entry into global perceptual networks. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.