Effects of quinine on neural activity in cat primary auditory cortex

Ochi, Kentaro; Eggermont, Jos J.

doi:10.1016/s0378-5955(96)00201-8

Cited by 80 publications

(58 citation statements)

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“…Using the cross-correlation technique, Eggermont and colleagues have also reported an increase in the degree of auditory synchronisation after application of quinine. In cat A1, quinine was shown to significantly increase the height of the peak of the correlation between the spontaneous activity recorded across separate electrodes (Ochi and Eggermont, 1997) in a dosedependent manner. In another study by Ochi and Eggermont (1996) a greater number of auditory neuron pairs showed significantly correlated firing after salicylate application in cat A1, however, the strength of the peak of correlation did not alter.…”

Section: Guidance From Animal Electrophysiological Studiesmentioning

confidence: 91%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

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Section: Guidance From Animal Electrophysiological Studiesmentioning

confidence: 91%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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“…Unfortunately, an unambiguous link between bursting and tinnitus has yet to emerge (Kaltenbach, 2000), and it is not clear if they are sustained for a long time. In addition, cross correlation of simultaneously recorded neuron activity in the primary auditory cortex (area AI), following noise exposure or quinine treatment, reveal an increase in synchronized discharges patterns (Noreña and Eggermont, 2003;Ochi and Eggermont, 1997). This emergence of synchronized activity (meaning that the SA of multiple neurons are occurring at the same time) is related to cortical reorganization and tends to increase with time.…”

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 98%

“…Neuroplastic events at the auditory cortex (AC) have been reported to include hyperactive SA of cortical neurons and an increase in neuronal synchronization (Noreña & Eggermont, 2003;Ochi & Eggermont, 1997;Seki & Eggermont, 2003). Recently a spiking neuron model of the AC was developed in which lateral excitation and loss of inhibition altered the strength of cortical connections causing increased SA and neuron synchrony (Dominguez, Becker, Bruce, & Read, 2006).…”

Section: Cortical Reorganization and Tinnitusmentioning

confidence: 99%

The role of central nervous system plasticity in tinnitus

Saunders

2007

Journal of Communication Disorders

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Tinnitus is a vexing disorder of hearing characterized by sound sensations originating in the head without any external stimulation. The specific etiology of these sensations is uncertain but frequently associated with hearing loss. The "neurophysiogical" model of tinnitus has enhanced appreciation of central nervous system (CNS) contributions. The model assumes that plastic changes in the primary and non-primary auditory pathways contribute to tinnitus with the former perhaps sustaining them, and the latter contributing to perceived severity and emotionality. These plastic changes are triggered by peripheral injury, which results in new patterns of brain activity due to anatomic alterations in the connectivity of CNS neurons. These alterations may change the balance between excitatory and inhibitory brain processes, perhaps producing cascades of new neural activity flowing between brainstem and cortex in a self-sustaining manner that produces persistent perceptions of tinnitus. The bases of this model are explored with an attempt to distinguish phenomenological from mechanistic explanations.Learning outcomes-(1) Readers will learn that the variables associated with the behavioral experience of tinnitus are as complex as the biological variables. (2) Readers will understand what the concept of neuroplastic brain change means, and how it is associated with tinnitus. (3) Readers will learn that there may be no one brain location associated with tinnitus, and it may result from interactions between multiple brain areas. (4) Readers will learn how disinhibition, spontaneous activity, neural synchronization, and tonotopic reorganization may contribute to tinnitus.

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“…noise exposure; tinnitus; spontaneous activity; dorsal cochlear nucleus ablation; tonotopic organization MANIPULATIONS THAT CAUSE TINNITUS in human subjects induce dramatic changes in the spontaneous discharge patterns of neurons in auditory centers of the brain. This has been shown in animal studies using acute tinnitus inducers, such as sodium salicylate and quinine (Chen and Jastreboff 1995; Eggermont and Kenmochi 1998;Manabe et al 1997;Ochi and Eggermont 1997), as well as inducers of chronic tinnitus, including excessive sound exposures (Brozoski et al 2002;Kaltenbach and McCaslin 1996;Kaltenbach et al 2000;Seki and Eggermont 2002) and platin drugs (Bauer et al 2008;Kaltenbach et al 2002). These treatments cause auditory centers to develop increased levels of bursting and nonbursting spontaneous activity (hyperactivity) and increased synchrony across the neural populations.…”

mentioning

confidence: 89%

“…Such changes have been well characterized at the multiunit and single-unit levels in structures as diverse as the dorsal cochlear nucleus (DCN) (Brozoski et al, 2002;Finlayson and Kaltenbach 2009;Kaltenbach and McCaslin 1996;Kaltenbach et al 2000Kaltenbach et al , 2002Middleton et al 2011;Shore et al 2008), the ventral cochlear nucleus (VCN) (Vogler et al 2011), the inferior colliculus (IC) (Bauer et al 2008;Chen and Jastreboff 1995;Dong et al 2009Dong et al , 2010aDong et al , 2010bJastreboff and Sasaki 1986;Mulders and Robertson 2009;Mulders et al 2010Wallhäusser-Franke et al 2003), and the auditory cortex (Eggermont and Kenmochi 1998;Eggermont 2005, 2006;Ochi and Eggermont 1997;Seki and Eggermont 2003;Wallhäusser-Franke et al 1996), suggesting that tinnitus may be a system-wide pathology. Indeed, functional imaging studies in both animals and human subjects with tinnitus show clear evidence of hyperactivation of centers both within and beyond the auditory system (Brozoski et al 2007;Eichhammer et al 2007;Langguth et al 2006;Lanting et al 2008;Lobarinas et al 2008;Lockwood et al 1998;Melcher et al 2000Melcher et al , 2009Reyes et al 2002).…”

mentioning

confidence: 99%

Noise-induced hyperactivity in the inferior colliculus: its relationship with hyperactivity in the dorsal cochlear nucleus

Manzoor

Licari

Klapchar

et al. 2012

Journal of Neurophysiology

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Manzoor NF, Licari F, Klapchar M, Elkin RL, Gao Y, Chen G, Kaltenbach JA. Noise-induced hyperactivity in the inferior colliculus: its relationship with hyperactivity in the dorsal cochlear nucleus. J Neurophysiol 108: 976 -988, 2012. First published May 2, 2012; doi:10.1152/jn.00833.2011.-Intense noise exposure causes hyperactivity to develop in the mammalian dorsal cochlear nucleus (DCN) and inferior colliculus (IC). It has not yet been established whether the IC hyperactivity is driven by hyperactivity from extrinsic sources that include the DCN or instead is maintained independently of this input. We have investigated the extent to which IC hyperactivity is dependent on input from the contralateral DCN by comparing recordings of spontaneous activity in the IC of noise-exposed and control hamsters before and after ablation of the contralateral DCN. One group of animals was binaurally exposed to intense sound (10 kHz, 115 dB SPL, 4 h), whereas the control group was not. Both groups were studied electrophysiologically 2-3 wk later by first mapping spontaneous activity along the tonotopic axis of the IC to confirm induction of hyperactivity. Spontaneous activity was then recorded at a hyperactive IC locus over two 30-min periods, one with DCNs intact and the other after ablation of the contralateral DCN. In a subset of animals, activity was again mapped along the tonotopic axis after the time course of the activity was recorded before and after DCN ablation. Following recordings, the brains were fixed, and histological evaluations were performed to assess the extent of DCN ablation. Ablation of the DCN resulted in major reductions of IC hyperactivity. Levels of postablation activity in exposed animals were similar to the levels of activity in the IC of control animals, indicating an almost complete loss of hyperactivity in exposed animals. The results suggest that hyperactivity in the IC is dependent on support from extrinsic sources that include and may even begin with the DCN. This finding does not rule out longer term compensatory or homeostatic adjustments that might restore hyperactivity in the IC over time. noise exposure; tinnitus; spontaneous activity; dorsal cochlear nucleus ablation; tonotopic organization MANIPULATIONS THAT CAUSE TINNITUS in human subjects induce dramatic changes in the spontaneous discharge patterns of neurons in auditory centers of the brain. This has been shown in animal studies using acute tinnitus inducers, such as sodium salicylate and quinine (Chen and Jastreboff 1995; Eggermont and Kenmochi 1998;Manabe et al. 1997;Ochi and Eggermont 1997), as well as inducers of chronic tinnitus, including excessive sound exposures (Brozoski et al. 2002;Kaltenbach and McCaslin 1996;Kaltenbach et al. 2000;Seki and Eggermont 2002) and platin drugs (Bauer et al. 2008;Kaltenbach et al. 2002). These treatments cause auditory centers to develop increased levels of bursting and nonbursting spontaneous activity (hyperactivity) and increased synchrony across the neural populations.Such changes have bee...

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Effects of quinine on neural activity in cat primary auditory cortex

Cited by 80 publications

References 37 publications

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

The role of central nervous system plasticity in tinnitus

Noise-induced hyperactivity in the inferior colliculus: its relationship with hyperactivity in the dorsal cochlear nucleus

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