Alterations in Average Spectrum of Cochleoneural Activity by Long-Term Salicylate Treatment in the Guinea Pig: A Plausible Index of Tinnitus

1998 ◽  
Vol 80 (4) ◽  
pp. 2113-2120 ◽  
Author(s):  
Y. Cazals ◽  
K. C. Horner ◽  
Z. W. Huang
Keyword(s):  
Hearing Loss ◽  
Guinea Pig ◽  
Auditory Nerve ◽  
Acoustic Noise ◽  
Compound Action Potential ◽  
Broadband Noise ◽  
Nerve Activity ◽  
Average Spectrum ◽  
Acoustic Tuning

Cazals, Y., K. C. Horner, and Z. W. Huang. Alterations in average spectrum of cochleoneural activity by long-term salicylate treatment in the guinea pig: a plausible index of tinnitus. J. Neurophysiol. 80: 2113–2120, 1998. Salicylate, one of the most widely used drugs, produces at repetitive high doses reversible tinnitus and hearing loss. Neural correlates of hearing loss have long been established, whereas they remain elusive for tinnitus. The average spectrum of electrophysiological cochleoneural activity (ASECA), a measure of spontaneous auditory nerve activity, was monitored in guinea pigs over weeks of salicylate administration. Auditory nerve compound action potential (CAP) was also recorded to monitor acoustic sensitivity. In the first days of treatment, ASECA decreased acutely during hours after salicylate administration; after several days this decrease could be reduced. Over weeks of treatment the level of ASECA increased progressively. No change in CAP threshold was observed. The ASECA decrease induced by a contralateral broadband noise remained unchanged. At the end of treatment, acoustic tuning of ASECA showed a partially decreased sensitivity. After cessation of treatment the ASECA level returned progressively to initial values. In control animals delivery of an ipsilateral acoustic noise could reproduce the ASECA increase observed in long-term salicylate-treated animals. This white noise was of moderate sound pressure level and it elevated slightly CAP thresholds at high frequencies. These data provide evidence for salicylate-induced ASECA alterations without changes in CAP thresholds, in accord with clinical reports of tinnitus being the first subjective sign of salicylate ototoxicity. The similarities in occurrence, development, reversibility, frequency content, and acoustic level support the idea that ASECA changes, which indicates alterations of spontaneous eighth nerve activity and reflects the presence of salicylate-induced high-pitch tinnitus.

scholarly journals Synaptic Transmission at the Cochlear Nucleus Endbulb Synapse During Age-Related Hearing Loss in Mice

2005 ◽  
Vol 94 (3) ◽  
pp. 1814-1824 ◽  
Author(s):  
Yong Wang ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Synaptic Transmission ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
High Frequency ◽  
Nerve Activity ◽  
Synaptic Release ◽  
Endbulb Of Held ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) typically starts from high-frequency regions of the cochlea and over time invades lower-frequency regions. During this progressive hearing loss, sound-evoked activity in spiral ganglion cells is reduced. DBA mice have an early onset of AHL. In this study, we examined synaptic transmission at the endbulb of Held synapse between auditory nerve fibers and bushy cells in the anterior ventral cochlear nucleus (AVCN). Synaptic transmission in hearing-impaired high-frequency areas of the AVCN was altered in old DBA mice. The spontaneous miniature excitatory postsynaptic current (mEPSC) frequency was substantially reduced (about 60%), and mEPSCs were significantly slower (about 115%) and smaller (about 70%) in high-frequency regions of old (average age 45 days) DBA mice compared with tonotopically matched regions of young (average age 22 days) DBA mice. Moreover, synaptic release probability was about 30% higher in high-frequency regions of young DBA than that in old DBA mice. Auditory nerve–evoked EPSCs showed less rectification in old DBA mice, suggesting recruitment of GluR2 subunits into the AMPA receptor complex. No similar age-related changes in synaptic release or EPSCs were found in age-matched, normal hearing young and old CBA mice. Taken together, our results suggest that auditory nerve activity plays a critical role in maintaining normal synaptic function at the endbulb of Held synapse after the onset of hearing. Auditory nerve activity regulates both presynaptic (release probability) and postsynaptic (receptor composition and kinetics) function at the endbulb synapse after the onset of hearing.

Additivity of loud-sound--induced threshold losses in the cat under conditions of active or inactive cochlear efferent-mediated protection

1996 ◽  
Vol 75 (4) ◽  
pp. 1601-1618 ◽  
Author(s):  
R. Rajan
Keyword(s):  
Hearing Loss ◽  
Guinea Pig ◽  
Compound Action Potential ◽  
Single Exposure ◽  
Initial Exposure ◽  
Loud Sound ◽  
Critical Observation ◽  
Pure Tones ◽  
Compound Action

1. An additivity model for the accretion of cochlear sensorineural hearing losses has been described from studies in the guinea pig cochlea. Among other aspects, the model allows determination of how residual hearing losses after an initial exposure (E1) affect hearing losses to be expected to a subsequent second exposure (E2). In the present study, the model was applied to temporary hearing losses produced in the cat cochlea by loud pure tones at a frequency from 3 to 15 kHz, affecting regions from 2 to 28 kHz. Successive identical exposures, generally with an interexposure interval of approximately equal to 35 min, were used to produce compound action potential (CAP) threshold losses. Total losses after E2 were compared with those predicted by the model. Testing was carried out under conditions where olivocochlear bundle (OCB)-mediated protection was or was not activated. (As shown elsewhere, OCB-mediated protection is activated by particular binaural exposures, but not monaural exposure, and reduces threshold losses in the binaural condition with intact OCB compared with losses in either the monaural condition, or the binaural condition where the OCB was cut before loud sound.) 2. The additivity model was a very good predictor of total losses under a variety of conditions; different exposure frequencies, monaural and binaural exposures, and with intact or cut OCB pathways. In these exposures, the model's application could be generalized so that as long as residual losses just pre-E2 were well specified in an animal, total losses could be as well predicted using normative data bases of a single exposure with the same parameters. 3. The model also allowed determination of whether OCB-mediated protection was exercised during E2 in dual identical exposures. Expression of protection for E2 depended on whether E1 elicited protection. When tested with monaural (at 7 or 15 kHz) or binaural exposures (at kHz) for which E1 did not elicit protection, neither did E2. However, when tested with a binaural E1 (at 7, 11, or 15 kHz), which activated protection, E2 also elicited protection. In the latter case, for 7- and 11-kHz exposures, the amount of E2 protection increased with total hearing loss, a relationship similar to that seen for single exposures in cat and guinea pig. For 15-kHz exposure, the amount of E2 protection was constant across test frequencies. 4. Finally, a critical observation with 11-kHz exposure was that a binaural E1 eliciting protection was able to "prime" the OCB so that protection could be elicited by a subsequent monaural E2, which, by itself as a singel exposure, does not evoke protection. This result has important implications in terms of the physiology of the protective OCB pathways and clinically in terms of the manner in which loud-sound-induced hearing loss accumulated.

scholarly journals Response Growth With Sound Level in Auditory-Nerve Fibers After Noise-Induced Hearing Loss

2004 ◽  
Vol 91 (2) ◽  
pp. 784-795 ◽  
Author(s):  
Michael G. Heinz ◽  
Eric D. Young
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Dynamic Range ◽  
Nerve Fibers ◽  
Sound Level ◽  
Broadband Noise ◽  
Noise Induced Hearing Loss ◽  
Rate Level

People with sensorineural hearing loss are often constrained by a reduced acoustic dynamic range associated with loudness recruitment; however, the neural correlates of loudness and recruitment are still not well understood. The growth of auditory-nerve (AN) activity with sound level was compared in normal-hearing cats and in cats with a noise-induced hearing loss to test the hypothesis that AN-fiber rate-level functions are steeper in impaired ears. Stimuli included best-frequency and fixed-frequency tones, broadband noise, and a brief speech token. Three types of impaired responses were observed. 1) Fibers with rate-level functions that were similar across all stimuli typically had broad tuning, consistent with outer-hair-cell (OHC) damage. 2) Fibers with a wide dynamic range and shallow slope above threshold often retained sharp tuning, consistent with primarily inner-hair-cell (IHC) damage. 3) Fibers with very steep rate-level functions for all stimuli had thresholds above approximately 80 dB SPL and very broad tuning, consistent with severe IHC and OHC damage. Impaired rate-level slopes were on average shallower than normal for tones, and were steeper in only limited conditions. There was less variation in rate-level slopes across stimuli in impaired fibers, presumably attributable to the lack of suppression-induced reductions in slopes for complex stimuli relative to BF-tone slopes. Sloping saturation was observed less often in impaired fibers. These results illustrate that AN fibers do not provide a simple representation of the basilar-membrane I/O function and suggest that both OHC and IHC damage can affect AN response growth.

Effects of conductive hearing loss on auditory nerve activity in gerbil

2002 ◽  
Vol 164 (1-2) ◽  
pp. 127-137 ◽  
Author(s):  
Raymond D. Cook ◽  
Thomas Y. Hung ◽  
Roger L. Miller ◽  
David W. Smith ◽  
Debara L. Tucci
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Conductive Hearing Loss ◽  
Nerve Activity ◽  
Conductive Hearing

scholarly journals Contrasting mechanisms for hidden hearing loss: synaptopathy vs myelin defects

2020 ◽  
Author(s):  
Maral Budak ◽  
Karl Grosh ◽  
Gabriel Corfas ◽  
Michal Zochowski ◽  
Victoria Booth
Keyword(s):  
Hearing Loss ◽  
Action Potential ◽  
Auditory Nerve ◽  
Compound Action Potential ◽  
Auditory Neuron ◽  
Type I ◽  
Noisy Environments ◽  
Hearing Thresholds ◽  
Hidden Hearing Loss ◽  
Compound Action

AbstractHidden hearing loss (HHL) is an auditory neuropathy characterized by normal hearing thresholds but reduced amplitude of the sound-evoked auditory nerve compound action potential (CAP). It has been proposed that in humans HHL leads to speech discrimination and intelligibility deficits, particularly in noisy environments. Animal models originally indicated that HHL can be caused by moderate noise exposures or aging, and that loss of inner hair cell (IHC) synapses could be its cause. A recent study provided evidence that transient loss of cochlear Schwann cells also causes permanent auditory deficits in mice which have characteristics of HHL. Histological analysis of the cochlea after auditory nerve remyelination showed a permanent disruption of the myelination patterns at the heminode of type I spiral ganglion neuron (SGN) peripheral terminals, suggesting that this defect could be contributing to HHL. To shed light on the mechanisms of different HHL scenarios and to test their impact on type I SGN activity, we constructed a reduced biophysical model for a population of SGN peripheral axons. We found that the amplitudes of simulated sound-evoked SGN CAPs are lower and have greater latencies when the heminodes are disorganized, i.e. they are placed at different distances from the hair cell rather than at the same distance as seen in the normal cochlea. Thus, our model confirms that disruption of the position of the heminode causes desynchronization of SGN spikes leading to a loss of temporal resolution and reduction of the sound-evoked SGN CAP. We also simulated synaptopathy by removing high threshold IHC-SGN synapses and found that the amplitude of simulated sound-evoked SGN CAPs decreases while latencies remain unchanged, corresponding to what has been observed in noise exposed animals. This model can be used to further study the effects of synaptopathy or demyelination on auditory function.Author summaryHidden hearing loss is an auditory disorder caused by noise exposure, aging or peripheral neuropathy which is estimated to affect 12-15% of the world’s population. It is a ‘hidden’ disorder because subjects have normal hearing thresholds, i.e., the condition cannot be revealed by standard audiological tests, but they report difficulties in understanding speech in noisy environments. Studies on animal models suggest two possible pathogenic mechanisms for hidden hearing loss: (1) loss of synapses between inner hair cells and auditory nerve fibers, and (2) disruption of auditory-nerve myelin. In this study, we constructed a computational model of sound-evoked auditory neuron fiber activity and auditory nerve compound action potential to understand how each one of these mechanisms affects nerve transmission. We show that disruption of auditory-nerve myelin desynchronizes sound-evoked auditory neuron spiking, decreasing the amplitude and increasing the latency of the compound action potential. In addition, elongation of the initial axon segment may cause spike generation failure leading to decreased spiking probability. In contrast, the effect of synapse loss is only to decrease the probability of firing, thus reducing the compound action potential amplitude without disturbing its latency. This model, which accurately represents the in vivo findings, could be useful to make further predictions on the consequences of HHL and extend it to explore the impact of synaptopathy and myelinopathy on hearing.

Age-Related and Noise-Induced Hearing Loss

2018 ◽  
pp. 162-188
Author(s):  
Ruili Xie ◽  
Tessa-Jonne F. Ropp ◽  
Michael R. Kasten ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Transmitter Release ◽  
Time Course ◽  
Functional Change ◽  
Noise Induced Hearing Loss ◽  
Nerve Activity ◽  
Auditory Periphery ◽  
Age Related ◽  
Age Related Hearing Loss

Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.

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