Generators of the brainstem auditory evoked potential in cat. II. Correlating lesion sites with waveform changes

Melcher, Jennifer R.; Guinan, John J.; Knudson, Inge M.; Kiang, N. Y. S.

doi:10.1016/0378-5955(95)00179-4

Cited by 114 publications

(64 citation statements)

References 41 publications

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“…In cat, for instance, focal lesioning within the cochlear nucleus has demonstrated that ABR waves subsequent to wave I are generated by pathways originating in the VCN (Gardi et al 1979;Achor and Starr 1980;Fullerton and Kiang 1990;Melcher et al 1996b). It has further indicated that two particular parallel pathways originating in VCN generate most, if not all, of the later ABR waves.…”

Section: Ventral Cochlear Nucleus and Tinnitusmentioning

confidence: 99%

“…Kehrle et al (2008) offered no direct interpretation. Shaette and McAlpine used a dorsal cochlear nucleus (DCN) model to interpret their finding of a V/I amplitude elevation despite evidence that the DCN and its output pathways make little or no contribution to the ABR (Gardi et al 1979;Achor and Starr 1980;Fullerton and Kiang 1990;Melcher et al 1996b). Here, we interpret the enhanced V/I and III/I amplitude ratios to elevated neuronal activity in a pathway through VCN.…”

Section: Comparison To Previous Abr Studies Of Tinnitusmentioning

confidence: 99%

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Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Herrmann

Levine

et al. 2012

JARO

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202

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Numerous studies have demonstrated elevated spontaneous and sound-evoked brainstem activity in animal models of tinnitus, but data on brainstem function in people with this common clinical condition are sparse. Here, auditory nerve and brainstem function in response to sound was assessed via auditory brainstem responses (ABR) in humans with tinnitus and without. Tinnitus subjects showed reduced wave I amplitude (indicating reduced auditory nerve activity) but enhanced wave V (reflecting elevated input to the inferior colliculi) compared with non-tinnitus subjects matched in age, sex, and puretone threshold. The transformation from reduced peripheral activity to central hyperactivity in the tinnitus group was especially apparent in the V/I and III/I amplitude ratios. Compared with a third cohort of younger, non-tinnitus subjects, both tinnitus, and matched, non-tinnitus groups showed elevated thresholds above 4 kHz and reduced wave I amplitude, indicating that the differences between tinnitus and matched non-tinnitus subjects occurred against a backdrop of shared peripheral dysfunction that, while not tinnitus specific, cannot be discounted as a factor in tinnitus development. Animal lesion and human neuroanatomical data combine to indicate that waves III and V in humans reflect activity in a pathway originating in the ventral cochlear nucleus (VCN) and with spherical bushy cells (SBC) in particular. We conclude that the elevated III/I and V/I amplitude ratios in tinnitus subjects reflect disproportionately high activity in the SBC pathway for a given amount of peripheral input. The results imply a role for the VCN in tinnitus and suggest the SBC pathway as a target for tinnitus treatment.

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Section: Ventral Cochlear Nucleus and Tinnitusmentioning

confidence: 99%

Section: Comparison To Previous Abr Studies Of Tinnitusmentioning

confidence: 99%

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Herrmann

Levine

et al. 2012

JARO

Self Cite

202

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“…The data suggest that both wave I and wave II are compound action potentials, with the former arising from the distal portion and the later from the proximal (brainstem) portion of the auditory nerve (Hashimoto et al, 1981;Møller and Jannetta 1981). The later waves are thought to have multiple generators, and are thought to have contributions from the superior olive and lemniscal pathways up to and including the inferior colliculus (Melcher et al, 1996a(Melcher et al, , 1996b(Melcher et al, , 1996c.…”

Section: The Auditory Brainstem Responsementioning

confidence: 99%

Auditory Neuropathy/Dys-synchrony and Its Perceptual Consequences

Rance

2005

Trends in Amplification

218

186

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Auditory neuropathy/dys-synchrony is a form of hearing impairment in which cochlear outer hair cell function is spared but neural transmission in the auditory pathway is disordered. This condition, or group of conditions with a common physiologic profile, accounts for approximately 7% of permanent childhood hearing loss and a significant (but as yet undetermined) proportion of adult impairment. This paper presents an overview of the mechanisms underlying auditory neuropathy/dys-synchrony-type hearing loss and the clinical profile for affected patients. In particular it examines the perceptual consequences of auditory neuropathy/dyssynchrony, which are quite different from those associated with sensorineural hearing loss, and considers currently available, and future management options.

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“…ABRs are averaged bioelectric potentials representing synchronous neural activity generated at several levels of the ascending auditory pathway. Cochlear nerve fibers contribute to the earliest wave, namely wave 1 (Melcher et al, 1996). DPOAEs arise as electrical distortions in electromechanical transduction, within the inner ear, that are reverse transduced into mechanical signals, amplified by OHCs, and then propagated back to the ear canal in which they can be measured in the sound pressure waveform (Lukashkin et al, 2002).…”

Section: Cochlear Thresholdsmentioning

confidence: 99%

Functional Role of GABAergic Innervation of the Cochlea: Phenotypic Analysis of Mice Lacking GABA_AReceptor Subunits α1, α2, α5, α6, β2, β3, or δ

Maison¹,

Rosahl²,

Homanics³

et al. 2006

J. Neurosci.

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The olivocochlear efferent system is both cholinergic and GABAergic and innervates sensory cells and sensory neurons of the inner ear. Cholinergic effects on cochlear sensory cells are well characterized, both in vivo and in vitro; however, the robust GABAergic innervation is poorly understood. To explore the functional roles of GABA in the inner ear, we characterized the cochlear phenotype of seven mouse lines with targeted deletion of a GABA A receptor subunit (␣1, ␣2, ␣5, ␣6, ␤2, ␤3, or ␦).

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Generators of the brainstem auditory evoked potential in cat. II. Correlating lesion sites with waveform changes

Cited by 114 publications

References 41 publications

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Auditory Neuropathy/Dys-synchrony and Its Perceptual Consequences

Functional Role of GABAergic Innervation of the Cochlea: Phenotypic Analysis of Mice Lacking GABA_AReceptor Subunits α1, α2, α5, α6, β2, β3, or δ

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Generators of the brainstem auditory evoked potential in cat. II. Correlating lesion sites with waveform changes

Cited by 114 publications

References 41 publications

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Auditory Neuropathy/Dys-synchrony and Its Perceptual Consequences

Functional Role of GABAergic Innervation of the Cochlea: Phenotypic Analysis of Mice Lacking GABAAReceptor Subunits α1, α2, α5, α6, β2, β3, or δ

Contact Info

Product

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Functional Role of GABAergic Innervation of the Cochlea: Phenotypic Analysis of Mice Lacking GABA_AReceptor Subunits α1, α2, α5, α6, β2, β3, or δ