Neural Hyperactivity of the Central Auditory System in Response to Peripheral Damage

Zhao, Yi; Song, Qiang; Li, Xinyi; Li, Chunyan

doi:10.1155/2016/2162105

Cited by 25 publications

(17 citation statements)

References 111 publications

(135 reference statements)

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“…We suggest that noise-exposed mice preserve or regain some auditory function through compensation in the central auditory system. Several studies have demonstrated increased central gain in response to peripheral damage ( Salvi et al, 2003 ; Gold and Bajo, 2014 ; Chambers et al, 2016 ; Clarkson et al, 2016 ; Möhrle et al, 2016 ; Zhao et al, 2016 ), although the underlying mechanisms remain uncertain ( Auerbach et al, 2014 ). This increase in gain is thought to partially compensate for the reduced sensory input.…”

Section: Discussionmentioning

confidence: 99%

Central Compensation in Auditory Brainstem after Damaging Noise Exposure

Schrode

Muniak

Kim

et al. 2018

eNeuro

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Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 amplitudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2–4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.

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Section: Discussionmentioning

confidence: 99%

Central Compensation in Auditory Brainstem after Damaging Noise Exposure

Schrode

Muniak

Kim

et al. 2018

eNeuro

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“…Development of hyperactivity in the auditory system in general and in particular in the IC following sound exposure is a complex, long lasting, and dynamic process (for review see Zhao et al, 2016 ). Immediately after exposure, spontaneous firing rates are elevated in DCN and VCN, whereas IC activity remains unchanged.…”

Section: Introductionmentioning

confidence: 99%

Effect of Unilateral Acoustic Trauma on Neuronal Firing Activity in the Inferior Colliculus of Mice

Hsiao

Galazyuk

2021

Front. Synaptic Neurosci.

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Neural hyperactivity induced by sound exposure often correlates with the development of hyperacusis and/or tinnitus. In laboratory animals, hyperactivity is typically induced by unilateral sound exposure to preserve one ear for further testing of hearing performance. Most ascending fibers in the auditory system cross into the superior olivary complex and then ascend contralaterally. Therefore, unilateral exposure should be expected to mostly affect the contralateral side above the auditory brain stem. On the other hand, it is well known that a significant number of neurons have crossing fibers at every level of the auditory pathway, which may spread the effect of unilateral exposure onto the ipsilateral side. Here we demonstrate that unilateral sound exposure causes development of hyperactivity in both the contra and ipsilateral inferior colliculus in mice. We found that both the spontaneous firing rate and bursting activity were increased significantly compared to unexposed mice. The neurons with characteristic frequencies at or above the center frequency of exposure showed the greatest increase. Surprisingly, this increase was more pronounced in the ipsilateral inferior colliculus. This study highlights the importance of considering both ipsi- and contralateral effects in future studies utilizing unilateral sound exposure.

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“…Many theories suggest that the underlying cause of tinnitus may be associated with damage to the sensory cochlear epithelium ( Henry et al, 2005 ), and if acute then this can be assessed in the patient by asking about the temporal association between noise exposure events, abrupt changes in hearing and tinnitus onset or exacerbation. In a review, Zhao et al (2016) found that specific insults to the peripheral auditory system (e.g., cochlear ablation, selective IHC or OHC loss, and mixed or incomplete IHC and OHC injuries) can all reduce cochlear output. The edge theory of tinnitus proposes having cochlear disturbance inducing tinnitus and caused by the shift of OHCs in the organ of Corti from the apical side toward the lesion in a high-frequency basal side ( Nuttal et al, 2004 ).…”

Section: Mechanisms Involved In Maintenance Of Tinnitusmentioning

confidence: 99%

Pathophysiology of Subjective Tinnitus: Triggers and Maintenance

et al. 2018

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Tinnitus is the conscious perception of a sound without a corresponding external acoustic stimulus, usually described as a phantom perception. One of the major challenges for tinnitus research is to understand the pathophysiological mechanisms triggering and maintaining the symptoms, especially for subjective chronic tinnitus. Our objective was to synthesize the published literature in order to provide a comprehensive update on theoretical and experimental advances and to identify further research and clinical directions. We performed literature searches in three electronic databases, complemented by scanning reference lists from relevant reviews in our included records, citation searching of the included articles using Web of Science, and manual searching of the last 6 months of principal otology journals. One-hundred and thirty-two records were included in the review and the information related to peripheral and central mechanisms of tinnitus pathophysiology was collected in order to update on theories and models. A narrative synthesis examined the main themes arising from this information. Tinnitus pathophysiology is complex and multifactorial, involving the auditory and non-auditory systems. Recent theories assume the necessary involvement of extra-auditory brain regions for tinnitus to reach consciousness. Tinnitus engages multiple active dynamic and overlapping networks. We conclude that advancing knowledge concerning the origin and maintenance of specific tinnitus subtypes origin and maintenance mechanisms is of paramount importance for identifying adequate treatment.

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Neural Hyperactivity of the Central Auditory System in Response to Peripheral Damage

Cited by 25 publications

References 111 publications

Central Compensation in Auditory Brainstem after Damaging Noise Exposure

Central Compensation in Auditory Brainstem after Damaging Noise Exposure

Effect of Unilateral Acoustic Trauma on Neuronal Firing Activity in the Inferior Colliculus of Mice

Pathophysiology of Subjective Tinnitus: Triggers and Maintenance

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