scholarly journals Phase Locking of Auditory Nerve Fibers: The Role of Lowpass Filtering by Hair Cells

2020 ◽  
Vol 40 (24) ◽  
pp. 4700-4714 ◽  
Author(s):  
Adam J. Peterson ◽  
Peter Heil
Keyword(s):  
Hair Cells ◽  
Auditory Nerve ◽  
Phase Locking ◽  
Nerve Fibers ◽  
Auditory Nerve Fibers ◽  
Lowpass Filtering

Pathophysiology of Tinnitus

1984 ◽  
Vol 93 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Aage R. Møsller
Keyword(s):  
Auditory Nerve ◽  
Neural Coding ◽  
Temporal Pattern ◽  
Phase Locking ◽  
Cranial Nerves ◽  
Nerve Fibers ◽  
Complex Sounds ◽  
Ephaptic Transmission ◽  
Recent Developments ◽  
Auditory Nerve Fibers

The hypothesis is presented that certain forms of tinnitus are related to abnormal phase-locking of discharges in groups of auditory nerve fibers. Recent developments in auditory neurophysiology have shown that neural coding of the temporal pattern of sounds plays an important role in the analysis of complex sounds. In addition, it has been demonstrated that when some other cranial nerves are damaged, artificial synapses can occur between individual nerve fibers such that ephaptic transmission between nerve fibers is facilitated. Such “crosstalk” between auditory nerve fibers is assumed to result in phase-locking of the spontaneous activity of groups of neurons which in the absence of external sounds creates a neural pattern that resembles that evoked by sounds.

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.

Spike timing in auditory-nerve fibers during spontaneous activity and phase locking

Synapse ◽  
2016 ◽  
Vol 71 (1) ◽  
pp. 5-36 ◽  
Author(s):  
Peter Heil ◽  
Adam J. Peterson
Keyword(s):  
Spontaneous Activity ◽  
Auditory Nerve ◽  
Phase Locking ◽  
Nerve Fibers ◽  
Spike Timing ◽  
Auditory Nerve Fibers

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.

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