Neuroscience
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Review
Age-related Changes in Neural Coding of Envelope Cues: Peripheral Declines and Central Compensation.
Aging listeners often experience difficulties in perceiving temporally complex acoustic cues in noisy environments. These difficulties likely have neurophysiological contributors from various levels of auditory processing. Cochlear synapses between inner hair cells and auditory nerve fibers exhibit a progressive decline with age which is not reflected in the threshold audiogram. ⋯ This results in a modulation frequency selective increase in the representation of envelope cues at the level of the auditory midbrain and cortex. These changes may be shaped by mechanisms such as decreased inhibitory neurotransmission occurring with age across various central auditory nuclei. Altered representations of the differing temporal components of speech due to these interactions between multiple levels of the auditory pathway may contribute to the age-related difficulties hearing speech in noisy environments.
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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.
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The effects of traumatic noise-exposure and deafening on auditory system function have received a great deal of attention. However, lower levels of noise as well as temporary conductive hearing loss also have consequences on auditory physiology and hearing. Here we review how abnormal acoustic experience at early ages affects the ascending and descending auditory pathways, as well as hearing behavior.
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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.