Synchronous auditory nerve activity in the carboplatin-chinchilla model of auditory neuropathy

Cowper-Smith, Christopher D.; Dingle, Rachel N.; Guo, Yong; Burkard, Robert; Phillips, Dennis P.

doi:10.1121/1.3453764

Cited by 9 publications

(7 citation statements)

References 23 publications

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“…Given that neural timing is suggested to reflect temporal jitter and synchronicity, these non-delayed latencies seen in the experimental group after hearing aid use could be interpreted as an increase in synchronicity and may be affected by an inhibition-mediated decrease in temporal jitter. Reduced input from the periphery due to hearing loss, changes neural responses in the inferior colliculus (Cowper-Smith et al, 2010). Reduced afferent neural transmission may be sufficient to desynchronize neural activity in the inferior colliculus and these reductions may destabilize the tight regulation of excitatory/inhibitory neurotransmission needed for temporal processing.…”

Section: Discussionmentioning

confidence: 99%

Neural and behavioral changes after the use of hearing aids

Karawani

Jenkins

Anderson

2018

Clinical Neurophysiology

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Section: Discussionmentioning

confidence: 99%

Neural and behavioral changes after the use of hearing aids

Karawani

Jenkins

Anderson

2018

Clinical Neurophysiology

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“…The chinchilla model has recently been used to test the hypothesis that reduced input from the periphery changes temporal responses of neurons in the inferior colliculus (Cowper-Smith et al, 2010). In the chinchilla, experimental treatment with carboplatin produces inner hair cell loss accompanied by loss of auditory nerve fibers and reduced spike rates of surviving fibers (Wake et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…In the chinchilla, experimental treatment with carboplatin produces inner hair cell loss accompanied by loss of auditory nerve fibers and reduced spike rates of surviving fibers (Wake et al, 1994). Cowper-Smith and colleagues (2010) showed that temporal responses of individual auditory nerve fibers and inferior colliculus neurons are similar in chinchilla before and after carboplatin treatment, suggesting that reduced afferent neural transmission is insufficient to desynchronize neural activity in the inferior colliculus, at least over the short term.…”

Section: Discussionmentioning

confidence: 99%

Age-Related Changes in the Auditory Brainstem Response

Konrad-Martin¹,

Dille²,

McMillan³

et al. 2012

J Am Acad Audiol

133

103

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Purpose This cross-sectional study had two goals: (1) Identify and quantify the effects of aging on the auditory brainstem response (ABR); (2) Describe how click rate and hearing impairment modify effects of aging. Research Design and Analysis ABR measures were obtained from 131 predominately male Veteran participants aged 26 to 71 yr. Metrics analyzed include amplitude and latency for waves I, III, and V, and the I–V interpeak latency interval (IPI) at three repetition rates (11, 51, and 71 clicks/sec) using both polarities. In order to avoid confounding from missing data due to hearing impairment, participants had hearing thresholds <40 dB HL at 2 kHz and 70 dB HL at 4 kHz in at least one ear. Additionally, the median 2, 3, and 4 kHz pure tone threshold average (PTA2,3,4) for the sample, ~17 dB HL, was used to delineate subgroups of better and worse hearing ears, and only the better hearing sample was modeled statistically. We modeled ABR responses using age, repetition rate, and PTA2,3,4 as covariates. Random effects were used to model correlation between the two ears of a subject and across repetition rates. Inferences regarding effects of aging on ABR measures at each rate were derived from the fitted model. Results were compared to data from subjects with poorer hearing. Results Aging substantially diminished amplitudes of all of the principal ABR peaks, largely independent of any threshold differences within the group. For waves I and III, age-related amplitude decrements were greatest at a low (11/sec) click rate. At the 11/sec rate, the model-based mean wave III amplitude was significantly smaller in older compared with younger subjects even after adjusting for wave I amplitude. Aging also increased ABR peak latencies, with significant shifts limited to early waves. The I–V IPI did not change with age. For both younger and older subjects, increasing click presentation rate significantly decreased amplitudes of early peaks and prolonged latencies of later peaks, resulting in increased IPIs. Advanced age did not enhance effects of rate. Instead, the rate effect on wave I and III amplitudes was attenuated for the older subjects due to reduced peak amplitudes at lower click rates. Compared with model predictions from the sample of better hearing subjects, mean ABR amplitudes were diminished in the group with poorer hearing, and wave V latencies were prolonged. Conclusions In a sample of veterans, aging substantially reduced amplitudes of all principal ABR peaks, with significant latency shifts limited to waves I and III. Aging did not influence the I–V IPI even at high click rates, suggesting that the observed absolute latency changes associated with aging can be attributed to changes in auditory nerve input. In contrast, ABR amplitude changes with age are not adequately explained by changes in wave I. Results suggest that aging reduces the numbers and/or synchrony of contributing auditory nerve units. Results also support the concept that aging reduces the numbers, though perhaps not the synchrony, ...

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“…This unique pathology was initially reported in the early 1990s; it was hoped that it would produce a model for AN 12 . However, detailed observation failed to show a loss of ANF synchrony in such animals 13 . Gene engineering models have been introduced for selective damage of SGNs.…”

Section: Introductionmentioning

confidence: 87%

Auditory Neuropathy after Damage to Cochlear Spiral Ganglion Neurons in Mice Resulting from Conditional Expression of Diphtheria Toxin Receptors

Pan

Song

Wang

et al. 2017

Sci Rep

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Auditory neuropathy (AN) is a hearing disorder characterized by normal cochlear amplification to sound but poor temporal processing and auditory perception in noisy backgrounds. These deficits likely result from impairments in auditory neural synchrony; such dyssynchrony of the neural responses has been linked to demyelination of auditory nerve fibers. However, no appropriate animal models are currently available that mimic this pathology. In this study, Cre-inducible diphtheria toxin receptor (iDTR +/+) mice were cross-mated with mice containing Cre (Bhlhb5-Cre +/−) specific to spiral ganglion neurons (SGNs). In double-positive offspring mice, the injection of diphtheria toxin (DT) led to a 30–40% rate of death for SGNs, but no hair cell damage. Demyelination types of pathologies were observed around the surviving SGNs and their fibers, many of which were distorted in shape. Correspondingly, a significant reduction in response synchrony to amplitude modulation was observed in this group of animals compared to the controls, which had a Cre− genotype. Taken together, our results suggest that SGN damage following the injection of DT in mice with Bhlhb5-Cre +/− and iDTR +/− is likely to be a good AN model of demyelination.

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Synchronous auditory nerve activity in the carboplatin-chinchilla model of auditory neuropathy

Cited by 9 publications

References 23 publications

Neural and behavioral changes after the use of hearing aids

Neural and behavioral changes after the use of hearing aids

Age-Related Changes in the Auditory Brainstem Response

Auditory Neuropathy after Damage to Cochlear Spiral Ganglion Neurons in Mice Resulting from Conditional Expression of Diphtheria Toxin Receptors

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