Behavioral Models of Tinnitus and Hyperacusis in Animals

Hayes, Sarah H.; Radziwon, Kelly E.; Stolzberg, Daniel; Salvi, Richard

doi:10.3389/fneur.2014.00179

Cited by 69 publications

(54 citation statements)

References 86 publications

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“…Both noise exposures used in this study increased sound-evoked hyperactivity in the AC and LA; these results are consistent with previous reports in which sound-evoked hyperactivity was observed in the AC and LA of rats with behavioral evidence of salicylate-induced hyperacusis (Chen et al, 2012, Chen et al, 2014b, Hayes et al, 2014, Chen et al, 2015). The noise-induced hyperactivity in AC and LA occurred in the low-frequency region of animals with high-frequency hearing loss; this would be expected to increase the loudness of low frequency sounds (low-frequency hyperacusis).…”

Section: Discussionsupporting

confidence: 93%

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

2016

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The effects of intense noise exposure on the classical auditory pathway have been extensively investigated; however, little is known about the effects of noise-induced hearing loss on non-classical auditory areas in the brain such as the lateral amygdala (LA) and striatum (Str). To address this issue, we compared the noise-induced changes in spontaneous and tone-evoked responses from multiunit clusters (MUC) in the LA and Str with those seen in auditory cortex (AC). High-frequency octave band noise (10–20 kHz) and narrow band noise (16–20 kHz) induced permanent thresho ld shifts (PTS) at high-frequencies within and above the noise band but not at low frequencies. While the noise trauma significantly elevated spontaneous discharge rate (SR) in the AC, SRs in the LA and Str were only slightly increased across all frequencies. The high-frequency noise trauma affected tone-evoked firing rates in frequency and time dependent manner and the changes appeared to be related to severity of noise trauma. In the LA, tone-evoked firing rates were reduced at the high-frequencies (trauma area) whereas firing rates were enhanced at the low-frequencies or at the edge-frequency dependent on severity of hearing loss at the high frequencies. The firing rate temporal profile changed from a broad plateau to one sharp, delayed peak. In the AC, tone-evoked firing rates were depressed at high frequencies and enhanced at the low frequencies while the firing rate temporal profiles became substantially broader. In contrast, firing rates in the Str were generally decreased and firing rate temporal profiles become more phasic and less prolonged. The altered firing rate and pattern at low frequencies induced by high frequency hearing loss could have perceptual consequences. The tone-evoked hyperactivity in low-frequency MUC could manifest as hyperacusis whereas the discharge pattern changes could affect temporal resolution and integration.

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Section: Discussionsupporting

confidence: 93%

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

2016

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“…In addition to inducing tinnitus with a putative pitch near 10–20 kHz (Brennan and Jastreboff, 1991; Kizawa et al, 2010; Lobarinas et al, 2004; Yang et al, 2007), our recent results show that high doses of SS also induce hyperacusis, a condition in which moderate intensity sounds are perceived as intolerably loud or painful (Chen et al, 2014a, 2015; Hayes et al, 2014). Our results from the AC indicate that SS-induced hyperactivity occurs over a broad frequency range (Fig.…”

Section: Discussionmentioning

confidence: 78%

Plastic changes along auditory pathway during salicylate-induced ototoxicity: Hyperactivity and CF shifts

et al. 2017

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High dose of salicylate, the active ingredient in aspirin, has long been known to induce transient hearing loss, tinnitus and hyperacusis making it a powerful experimental tool. These salicylate-induced perceptual disturbances are associated with a massive reduction in the neural output of the cochlea. Paradoxically, the diminished neural output of the cochlea is accompanied by a dramatic increase in sound-evoked activity in the auditory cortex (AC) and several other parts of the central nervous system. Exactly where the increase in neural activity begins and builds up along the central auditory pathway are not fully understood. To address this issue, we measured sound-evoked neural activity in the cochlea, cochlear nucleus (CN), inferior colliculus (IC), and AC before and after administering a high dose of sodium salicylate (SS, 300 mg/kg). The SS-treatment abolished low-level sound-evoked responses along the auditory pathway resulting in a 20–30 dB threshold shift. While the neural output of the cochlea was substantially reduced at high intensities, the neural responses in the CN were only slightly reduced; those in the IC were nearly normal or slightly enhanced while those in the AC considerably enhanced, indicative of a progress increase in central gain. The SS-induced increase in central response in the IC and AC was frequency-dependent with the greatest increase occurring in the mid-frequency range the putative pitch of SS-induced tinnitus. This frequency-dependent hyperactivity appeared to result from shifts in the frequency receptive fields (FRF) such that the response areas of many FRF shifted/expanded toward the mid-frequencies. Our results suggest that the SS-induced threshold shift originates in the cochlea. In contrast, enhanced central gain is not localized to one region, but progressively builds up at successively higher stage of the auditory pathway either through a loss of inhibition and/or increased excitation.

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“…Many animal studies using GPIAS and other models of tinnitus have used noise-exposure levels that induce TTS not PTS, so that functional hearing is preserved. While the validity of animal models is not without challenge [35–37], an increasing number of studies are demonstrating the usefulness of these procedures by providing consistent neurophysiological patterns in animals that express behavioral evidence of tinnitus as compared to those that do not, when all animals have been treated similarly. The findings give greater assurance that neural changes are being measured that are inextricably related to tinnitus, and that the changes can be differentiated from those that may relate only to hearing loss or hyperacusis.…”

Section: Properties Of Tinnitus Related To Audiometric Hearing Lossmentioning

confidence: 99%

Maladaptive plasticity in tinnitus — triggers, mechanisms and treatment

2016

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Tinnitus is a phantom auditory sensation that reduces quality of life for millions worldwide and for which there is no medical cure. Most cases are associated with hearing loss caused by the aging process or noise exposure. Because exposure to loud recreational sound is common among youthful populations, young persons are at increasing risk. Head or neck injuries can also trigger the development of tinnitus, as altered somatosensory input can affect auditory pathways and lead to tinnitus or modulate its intensity. Emotional and attentional state may play a role in tinnitus development and maintenance via top-down mechanisms. Thus, military in combat are particularly at risk due to combined hearing loss, somatosensory system disturbances and emotional stress. Neuroscience research has identified neural changes related to tinnitus that commence at the cochlear nucleus and extend to the auditory cortex and brain regions beyond. Maladaptive neural plasticity appears to underlie these neural changes, as it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures that may generate the phantom percept. This review highlights the links between animal and human studies, including several therapeutic approaches that have been developed, which aim to target the neuroplastic changes underlying tinnitus.

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Behavioral Models of Tinnitus and Hyperacusis in Animals

Cited by 69 publications

References 86 publications

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

Plastic changes along auditory pathway during salicylate-induced ototoxicity: Hyperactivity and CF shifts

Maladaptive plasticity in tinnitus — triggers, mechanisms and treatment

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