Temporal processing in inferior colliculus and auditory cortex affected by high doses of salicylate

Deng, Anchun; Lu, Jiong; Sun, Wei

doi:10.1016/j.brainres.2010.04.077

Cited by 17 publications

(14 citation statements)

References 44 publications

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“…The neural hyperactivity and frequency map reorganization that occurs in the central auditory center after treatment with high dose SS have been documented previously (Chen and Jastreboff, 1995; Chen et al, 2012, 2013, 2014a, 2014b; Deng et al, 2010; Lu et al, 2011; Norena et al, 2010; Stolzberg et al, 2011b; Sun et al, 2009; Zhang et al, 2011). However, the neural origins of these phenomena and the extent to which more peripheral structures such as the CN and IC contribute to these changes are poorly understood.…”

Section: Discussionsupporting

confidence: 57%

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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Section: Discussionsupporting

confidence: 57%

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

et al. 2017

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“…For example, enhanced driven neural activity is consistently observed across the tonotopic extent of the cortical surface even when salicylate is administered by different routes, such as systemically (Qiu et al, 2000; Yang et al, 2007; Sun et al, 2009a; Deng et al, 2010; Noreña et al, 2010; Lu et al, 2011; Zhang et al, 2011) (Figure 3), or directly to the cortical surface (Lu et al, 2011)—the latter approach being unlikely to bring about changes within the cochlea itself. The likelihood that this stably inducible effect is mediated via a suppression of GABAergic signaling efficacy is strongly suggested by the absence of any such enhancement when agents that positively modulate GABA pharmacology were coadministered (Sun et al, 2009a; Lu et al, 2011).…”

Section: Neuronal Spontaneous and Evoked Response Properties Undergo mentioning

confidence: 99%

“…In these experiments, recorded units displayed substantially broadened bandwidths, implying that a large degree of their sensitivity to pre-exposure CFs was presumably retained (Stolzberg et al, 2011). It is also rather striking that both salicylate exposure (Deng et al, 2010) and acoustic trauma (Yin et al, 2008) each yield an apparently equivalent reduction in the cortical gap-detection threshold for stimulation off-channel, i.e., completely outside of the region displaying peripheral threshold elevation. This might suggest that each insult commonly disrupts a frequency-insensitive mechanism, or mechanisms, critical to the precise encoding of temporally salient information.…”

Section: Insult-mediated Changes In Neural Spectrotemporal Receptive mentioning

confidence: 99%

“…This variable expression of neural excitability is almost certainly related to the plasticity phenotype of animals in various insult conditions. Indeed, systemic salicylate injection, which is understood to affect neural excitability (see above), has been recognized as effective in similarly modulating the suppression efficacy, largely in parallel with upregulation of neural gain in the auditory cortex (Deng et al, 2010; Sun et al, 2014). …”

Section: The Functional and Behavioral Implications Of Trauma-driven mentioning

confidence: 99%

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Insult-induced adaptive plasticity of the auditory system

Gold

Bajo

2014

Front. Neurosci.

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The brain displays a remarkable capacity for both widespread and region-specific modifications in response to environmental challenges, with adaptive processes bringing about the reweighing of connections in neural networks putatively required for optimizing performance and behavior. As an avenue for investigation, studies centered around changes in the mammalian auditory system, extending from the brainstem to the cortex, have revealed a plethora of mechanisms that operate in the context of sensory disruption after insult, be it lesion-, noise trauma, drug-, or age-related. Of particular interest in recent work are those aspects of auditory processing which, after sensory disruption, change at multiple—if not all—levels of the auditory hierarchy. These include changes in excitatory, inhibitory and neuromodulatory networks, consistent with theories of homeostatic plasticity; functional alterations in gene expression and in protein levels; as well as broader network processing effects with cognitive and behavioral implications. Nevertheless, there abounds substantial debate regarding which of these processes may only be sequelae of the original insult, and which may, in fact, be maladaptively compelling further degradation of the organism's competence to cope with its disrupted sensory context. In this review, we aim to examine how the mammalian auditory system responds in the wake of particular insults, and to disambiguate how the changes that develop might underlie a correlated class of phantom disorders, including tinnitus and hyperacusis, which putatively are brought about through maladaptive neuroplastic disruptions to auditory networks governing the spatial and temporal processing of acoustic sensory information.

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“…Hearing loss can potentially affect the outcome of GPIAS screening in a number ways: by interfering with audibility of the background sound in which the silent gaps are imbedded or by altering the amplitude of the startle reflex to the startle stimulus alone (no-gap condition). Previous studies in both rodents (55) and humans (56) have demonstrated that hearing loss alone, induced by sodium salicylate exposure, can interfere in detection of gaps in low-level continuous noise. This issue has been addressed in the GPIAS paradigm by using intensities of background sounds (60 dB SPL) shown to be resilient to the effects of hearing loss, and by carrying out noise-burst pre-pulse detection measures.…”

Section: Animal Models Of Tinnitusmentioning

confidence: 99%

Behavioral Models of Tinnitus and Hyperacusis in Animals

et al. 2014

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The phantom perception of tinnitus and reduced sound-level tolerance associated with hyperacusis have a high comorbidity and can be debilitating conditions for which there are no widely accepted treatments. One factor limiting the development of treatments for tinnitus and hyperacusis is the lack of reliable animal behavioral models of these disorders. Therefore, the purpose of this review is to highlight the current animal models of tinnitus and hyperacusis, and to detail the advantages and disadvantages of each paradigm. To date, this is the first review to include models of both tinnitus and hyperacusis.

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Temporal processing in inferior colliculus and auditory cortex affected by high doses of salicylate

Cited by 17 publications

References 44 publications

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

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

Insult-induced adaptive plasticity of the auditory system

Behavioral Models of Tinnitus and Hyperacusis in Animals

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