Responses of auditory nerve fibers innervating regenerated hair cells after local application of gentamicin at the round window of the cochlea in the pigeon

1999 ◽  
Vol 131 (1-2) ◽  
pp. 153-169 ◽  
Author(s):  
Marcus Müller ◽  
Jean W.T Smolders
Keyword(s):  
Hair Cells ◽  
Auditory Nerve ◽  
Round Window ◽  
Nerve Fibers ◽  
Local Application ◽  
Auditory Nerve Fibers

Contribution of auditory nerve fibers to compound action potential of the auditory nerve

2014 ◽  
Vol 112 (5) ◽  
pp. 1025-1039 ◽  
Author(s):  
Jérôme Bourien ◽  
Yong Tang ◽  
Charlène Batrel ◽  
Antoine Huet ◽  
Marc Lenoir ◽  
...  
Keyword(s):  
Action Potential ◽  
Auditory Nerve ◽  
Computational Simulation ◽  
Round Window ◽  
Hearing Threshold ◽  
Compound Action Potential ◽  
Nerve Fibers ◽  
Auditory Nerve Fibers ◽  
Round Window Niche ◽  
Compound Action

Sound-evoked compound action potential (CAP), which captures the synchronous activation of the auditory nerve fibers (ANFs), is commonly used to probe deafness in experimental and clinical settings. All ANFs are believed to contribute to CAP threshold and amplitude: low sound pressure levels activate the high-spontaneous rate (SR) fibers, and increasing levels gradually recruit medium- and then low-SR fibers. In this study, we quantitatively analyze the contribution of the ANFs to CAP 6 days after 30-min infusion of ouabain into the round window niche. Anatomic examination showed a progressive ablation of ANFs following increasing concentration of ouabain. CAP amplitude and threshold plotted against loss of ANFs revealed three ANF pools: 1) a highly ouabain-sensitive pool, which does not participate in either CAP threshold or amplitude, 2) a less sensitive pool, which only encoded CAP amplitude, and 3) a ouabain-resistant pool, required for CAP threshold and amplitude. Remarkably, distribution of the three pools was similar to the SR-based ANF distribution (low-, medium-, and high-SR fibers), suggesting that the low-SR fiber loss leaves the CAP unaffected. Single-unit recordings from the auditory nerve confirmed this hypothesis and further showed that it is due to the delayed and broad first spike latency distribution of low-SR fibers. In addition to unraveling the neural mechanisms that encode CAP, our computational simulation of an assembly of guinea pig ANFs generalizes and extends our experimental findings to different species of mammals. Altogether, our data demonstrate that substantial ANF loss can coexist with normal hearing threshold and even unchanged CAP amplitude.

scholarly journals Spatiotemporal Developmental Upregulation of Prestin Correlates With the Severity and Location of Cyclodextrin-Induced Outer Hair Cell Loss and Hearing Loss

2021 ◽  
Vol 9 ◽  
Author(s):  
Dalian Ding ◽  
Haiyan Jiang ◽  
Senthilvelan Manohar ◽  
Xiaopeng Liu ◽  
Li Li ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
High Frequency ◽  
Spiral Ganglion ◽  
Low Frequency ◽  
Nerve Fibers ◽  
Spiral Ganglion Neurons ◽  
Auditory Nerve Fibers ◽  
Ganglion Neurons

2-Hyroxypropyl-beta-cyclodextrin (HPβCD) is being used to treat Niemann-Pick C1, a fatal neurodegenerative disease caused by abnormal cholesterol metabolism. HPβCD slows disease progression, but unfortunately causes severe, rapid onset hearing loss by destroying the outer hair cells (OHC). HPβCD-induced damage is believed to be related to the expression of prestin in OHCs. Because prestin is postnatally upregulated from the cochlear base toward the apex, we hypothesized that HPβCD ototoxicity would spread from the high-frequency base toward the low-frequency apex of the cochlea. Consistent with this hypothesis, cochlear hearing impairments and OHC loss rapidly spread from the high-frequency base toward the low-frequency apex of the cochlea when HPβCD administration shifted from postnatal day 3 (P3) to P28. HPβCD-induced histopathologies were initially confined to the OHCs, but between 4- and 6-weeks post-treatment, there was an unexpected, rapid and massive expansion of the lesion to include most inner hair cells (IHC), pillar cells (PC), peripheral auditory nerve fibers, and spiral ganglion neurons at location where OHCs were missing. The magnitude and spatial extent of HPβCD-induced OHC death was tightly correlated with the postnatal day when HPβCD was administered which coincided with the spatiotemporal upregulation of prestin in OHCs. A second, massive wave of degeneration involving IHCs, PC, auditory nerve fibers and spiral ganglion neurons abruptly emerged 4–6 weeks post-HPβCD treatment. This secondary wave of degeneration combined with the initial OHC loss results in a profound, irreversible hearing loss.

Biomechanics of Hearing Sensitivity

1991 ◽  
Vol 113 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Sir James Lighthill
Keyword(s):  
Hair Cells ◽  
Auditory Nerve ◽  
Basilar Membrane ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Hearing Sensitivity ◽  
Sound Levels ◽  
Auditory Nerve Fibers ◽  
The Brain ◽  
Stiffness Distribution

This survey lecture on the biomechanics of hearing sensitivity is concerned, not with how the brain in man and other mammals analyzes the data coming to it along auditory nerve fibers, but with the initial capture of that data in the cochlea. The brain, needless to say, can produce all its miracles of interpretation only where it works on good initial data. For frequency selectivity these depend on some remarkable properties of the cochlea as a passive macromechanical system, comprising the basilar membrane with its steeply graded stiffness distribution vibrating within the cochlear fluids. But the biomechanics of hearing sensitivity to low levels of sound (at any particular frequency) calls also into play an active micromechanical system, which during the past few years has progressively been identified as located in the outer hair cells, and which, through a process of positive feedback, amplifies (in healthy ears) that basilar membrane vibration. This in turn offers the inner hair cells an enhanced signal at low sound levels, so that the threshold at which they can generate activity in auditory nerve fibers is, in consequence, very substantially lowered.

scholarly journals Probing adaptation and spontaneous firing in human auditory-nerve fibers with far-field peri-stimulus time responses

2021 ◽  
Author(s):  
Antoine Huet ◽  
Charlène Batrel ◽  
Xavier Dubernard ◽  
Jean-Charles Kleiber ◽  
Gilles Desmadryl ◽  
...  
Keyword(s):  
Auditory Nerve ◽  
Round Window ◽  
Nerve Fibers ◽  
Electrical Signal ◽  
Cochlear Nerve ◽  
Spontaneous Discharge ◽  
Rapid Adaptation ◽  
Discharge Rates ◽  
Auditory Nerve Fibers ◽  
Stimulus Time

AbstractInformation in sound stimuli is conveyed from sensory hair cells to the cochlear nuclei by the firing of auditory nerve fibers (ANFs). For obvious ethical reasons, single unit recordings from the cochlear nerve have never been performed in human, thus functional hallmarks of ANFs are unknown. By filtering and rectifying the electrical signal recorded at the round window of gerbil cochleae, we reconstructed a peri-stimulus time response (PSTR), with a waveform similar to the peri-stimulus time histograms (PSTHs) recorded from single ANFs. Pair-by-pair analysis of simultaneous PSTR and PSTH recordings in gerbil provided a model to predict the rapid adaptation and spontaneous discharge rates (SR) in a population of ANFs according to their location in the cochlea. We then probed the model in the mouse, in which the SR-based distribution of ANFs differs from the gerbil. We show that the PSTR-based predictions of the rapid adaptation time constant and mean SR across frequency again matched those obtained by recordings from single ANFs. Using PSTR recorded from the human cochlear nerve in 8 normal-hearing patients who underwent cerebellopontine angle surgeries for a functional cranial-nerve disorders (trigeminal neuralgia or hemifacial spasm), we predicted a rapid adaptation of about 3 milliseconds and a mean SR of 23 spikes/s in the 4 kHz frequency range in human ANFs. Together, our results support the use of PSTR as a promising diagnostic tool to map the auditory nerve in humans, thus opening new avenues to better understanding neuropathies, tinnitus, and hyperacusis.

The antidromic compound action potential of the auditory nerve

1994 ◽  
Vol 71 (5) ◽  
pp. 1826-1834 ◽  
Author(s):  
M. C. Brown
Keyword(s):  
Action Potential ◽  
Auditory Nerve ◽  
Refractory Period ◽  
Round Window ◽  
Compound Action Potential ◽  
Nerve Fibers ◽  
Negative Peak ◽  
Positive Peak ◽  
Auditory Nerve Fibers ◽  
Compound Action

1. The antidromic compound action potential (ACAP) of the auditory nerve was evoked by shocks to the auditory nerve root and recorded at the round window of the cochlea in anesthetized guinea pigs. The goal of this study was to determine the characteristics of the ACAP and compare these characteristics with those of the orthodromic, sound-evoked compound action potential (CAP). 2. The ACAP consists of an initial complex of a positive peak (p1) followed by a negative peak (n1). In contrast, the CAP consists of a negative peak (N1) followed by a positive peak (P1). These differences in waveform are likely due to the differences in conduction direction, antidromic for the ACAP vs. orthodromic for the CAP. 3. After the initial complex, the ACAP has a second complex of peaks (p2, n2) at a latency of approximately 1 ms; this complex is much smaller in amplitude than the initial complex (p1, n1). It is likely that the initial ACAP complex reflects firing of auditory-nerve fibers whereas the second complex reflects firing of neurons further centrally, perhaps in the cochlear nucleus, that are activated by orthodromic firing of auditory-nerve fibers. 4. Experiments with shock pairs are consistent with the idea that for auditory nerve fibers, the absolute refractory period is < 0.5 ms, and the relative refractory period is between 0.5 and at least 5 ms. 5. Experiments with click-shock pairs indicate that a shock interferes with the response to a click when the click and shock are given at about the same time.(ABSTRACT TRUNCATED AT 250 WORDS)

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