How 'hidden hearing loss' noise exposure affects neural coding in the inferior colliculus of rats.

Exposure to brief, intense sound can produce profound changes in the auditory system, from the internal structure of inner hair cells to reduced synaptic connections between the auditory nerves and the inner hair cells. Moreover, noisy environments can also lead to alterations in the auditory nerve or to processing changes in the auditory midbrain, all without affecting hearing thresholds. This so-called hidden hearing loss (HHL) has been shown in tinnitus patients and has been posited to account for hearing difficulties in noisy environments.

Characterizing subcutaneous cortical auditory evoked potentials in mice.

Auditory Brainstem Responses (ABRs) are a reliably robust measure of auditory thresholds in the mammalian hearing system and can be used to determine deficits in the auditory periphery. However, because these measures are limited to the lower stages of the auditory pathway, they are insensitive to changes or deficits that occur in the thalamic and cortical regions. Cortical Auditory Evoked Potentials (CAEPs), as longer latency responses, capture information from these regions.

Threshold Equalizing Noise Test Reveals Suprathreshold Loss of Hearing Function, Even in the "Normal" Audiogram Range.

Objectives: The threshold equalizing noise (TEN(HL)) is a clinically administered test to detect cochlear "dead regions" (i.e., regions of loss of inner hair cell [IHC] connectivity), using a "pass/fail" criterion based on the degree of elevation of a masked threshold in a tone-detection task.

Spontaneous Mouse Behavior in Presence of Dissonance and Acoustic Roughness.

According to a novel hypothesis (Arnal et al., 2015, Current Biology 25:2051-2056), auditory roughness, or temporal envelope modulations between 30 and 150 Hz, are present in both natural and artificial human alarm signals, which boosts the detection of these alarms in various tasks. These results also shed new light on the unpleasantness of dissonant sounds to humans, which builds upon the high level of roughness present in such sounds.

GABA receptors contribute more to rate than temporal coding in the IC of awake mice.

Speech is our most important form of communication, yet we have a poor understanding of how communication sounds are processed by the brain. Mice make great model organisms to study neural processing of communication sounds because of their rich repertoire of social vocalizations and because they have brain structures analogous to humans, such as the auditory midbrain nucleus inferior colliculus (IC). Although the combined roles of GABAergic and glycinergic inhibition on vocalization selectivity in the IC have been studied to a limited degree, the discrete contributions of GABAergic inhibition have only rarely been examined.

Localized disorganization of the cochlear inner hair cell synaptic region after noise exposure.

The prevalence and importance of hearing damage caused by noise levels not previously thought to cause permanent hearing impairment has become apparent in recent years. The damage to, and loss of, afferent terminals of auditory nerve fibres at the cochlear inner hair cell has been well established, but the effects of noise exposure and terminal loss on the inner hair cell are less known. Using three-dimensional structural studies in mice we have examined the consequences of afferent terminal damage on inner hair cell morphology and intracellular structure.

Hidden hearing loss selectively impairs neural adaptation to loud sound environments.

Exposure to even a single episode of loud noise can damage synapses between cochlear hair cells and auditory nerve fibres, causing hidden hearing loss (HHL) that is not detected by audiometry. Here we investigate the effects of noise-induced HHL on functional hearing by measuring the ability of neurons in the auditory midbrain of mice to adapt to sound environments containing quiet and loud periods. Neurons from noise-exposed mice show less capacity for adaptation to loud environments, convey less information about sound intensity in those environments, and adaptation to the longer-term statistical structure of fluctuating sound environments is impaired.

The Noise Exposure Structured Interview (NESI): An Instrument for the Comprehensive Estimation of Lifetime Noise Exposure.

Lifetime noise exposure is generally quantified by self-report. The accuracy of retrospective self-report is limited by respondent recall but is also bound to be influenced by reporting procedures. Such procedures are of variable quality in current measures of lifetime noise exposure, and off-the-shelf instruments are not readily available.

Increased spontaneous firing rates in auditory midbrain following noise exposure are specifically abolished by a Kv3 channel modulator.

Noise exposure has been shown to produce long-lasting increases in spontaneous activity in central auditory structures in animal models, and similar pathologies are thought to contribute to clinical phenomena such as hyperacusis or tinnitus in humans. Here we demonstrate that multi-unit spontaneous neuronal activity in the inferior colliculus (IC) of mice is significantly elevated four weeks following noise exposure at recording sites with frequency tuning within or near the noise exposure band, and this selective central auditory pathology can be normalised through administration of a novel compound that modulates activity of Kv3 voltage-gated ion channels. The compound had no statistically significant effect on IC spontaneous activity without noise exposure, nor on thresholds or frequency tuning of tone-evoked responses either with or without noise exposure.

Non-Monotonic Relation between Noise Exposure Severity and Neuronal Hyperactivity in the Auditory Midbrain.

The occurrence of tinnitus can be linked to hearing loss in the majority of cases, but there is nevertheless a large degree of unexplained heterogeneity in the relation between hearing loss and tinnitus. Part of the problem might be that hearing loss is usually quantified in terms of increased hearing thresholds, which only provides limited information about the underlying cochlear damage. Moreover, noise exposure that does not cause hearing threshold loss can still lead to "hidden hearing loss" (HHL), i.