Degeneration of auditory nerve fibers in guinea pigs with severe sensorineural hearing loss

2017 ◽  
Vol 345 ◽  
pp. 79-87 ◽  
Author(s):  
Steven Kroon ◽  
Dyan Ramekers ◽  
Emma M. Smeets ◽  
Ferry G.J. Hendriksen ◽  
Sjaak F.L. Klis ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Guinea Pigs ◽  
Nerve Fibers ◽  
Sensorineural Hearing ◽  
Auditory Nerve Fibers

A Spiking Neuron Model of Cortical Correlates of Sensorineural Hearing Loss: Spontaneous Firing, Synchrony, and Tinnitus

2006 ◽  
Vol 18 (12) ◽  
pp. 2942-2958 ◽  
Author(s):  
Melissa Dominguez ◽  
Suzanna Becker ◽  
Ian Bruce ◽  
Heather Read
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Neuron Model ◽  
Nerve Fibers ◽  
Sensorineural Hearing ◽  
Spontaneous Firing ◽  
Spiking Neuron ◽  
Spiking Neuron Model

Hearing loss due to peripheral damage is associated with cochlear hair cell damage or loss and some retrograde degeneration of auditory nerve fibers. Surviving auditory nerve fibers in the impaired region exhibit elevated and broadened frequency tuning, and the cochleotopic representation of broadband stimuli such as speech is distorted. In impaired cortical regions, increased tuning to frequencies near the edge of the hearing loss coupled with increased spontaneous and synchronous firing is observed. Tinnitus, an auditory percept in the absence of sensory input, may arise under these circumstances as a result of plastic reorganization in the auditory cortex. We present a spiking neuron model of auditory cortex that captures several key features of cortical organization. A key assumption in the model is that in response to reduced afferent excitatory input in the damaged region, a compensatory change in the connection strengths of lateral excitatory and inhibitory connections occurs. These changes allow the model to capture some of the cortical correlates of sensorineural hearing loss, including changes in spontaneous firing and synchrony; these phenomena may explain central tinnitus. This model may also be useful for evaluating procedures designed to segregate synchronous activity underlying tinnitus and for evaluating adaptive hearing devices that compensate for selective hearing loss.

scholarly journals Possibility of using embryonic neural cells to regenerate structures of the inner ear of Guinea pigs after experimental ototoxicosis

2021 ◽  
Vol 16 (2) ◽  
pp. 178-183
Author(s):  
Iryna Ihorivna SAPIZHAK ◽  
◽  
V. PYSANKO ◽  
T. MALYSHEVA ◽  
◽  
...  
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Inner Ear ◽  
Hearing Aids ◽  
Auditory Nerve ◽  
Guinea Pigs ◽  
Experimental Studies ◽  
Sensorineural Hearing ◽  
Neuronal Stem Cell ◽  
Morphological State

Hearing disorders greatly impair the comfort of life, change a person's emotional state, and when developed in early childhood lead to disorders of psycho-social formation of personality. There are currently no effective treatments for patients with sensorineural hearing loss (SNHL). Therefore, all over the world prefer "substitution tactics", namely - hearing aids for deafness, or cochlear implant for deafness. Aim. To evaluate the influence of NEC in different ways of their introduction on the morphological state of the structures of the inner ear (Corti's organ and the first neuron, vascular strip), as well as the auditory nerve on the background of aminoglycoside ototoxicosis. To investigate the characteristics and directions of reorganization of hemoblood supply and features of cyto - and myeloarchitectonics of structures of the inner ear. Materials and methods. To study the effectiveness of neuronal embryonic cells (NEC) in aminoglycoside ototoxicosis, experimental studies were performed on 40 guinea pigs weighing from 500 to 600 g. SNHL was caused by the introduction of aminoglycoside antibiotic - gentamicin sulfate at a dose of 100 mg/kg for 14 days. The neuronal stem cell suspension was administered in a volume of 2 million cells in 0.5 ml intratympanically and 2 million cells in 0.5 ml suboccipitally on days 1 and 15 of the experiment. Results and discussion. The influence of NEC on different methods of their introduction on the morphological state of the structures of the inner ear (Corti's organ and the first neuron), as well as the auditory nerve on the background of aminoglycoside ototoxicosis was evaluated. The characteristics and directions of reorganization of hemoblood supply and features of cyto - and myeloarchitectonics of structures of an inner ear according to an estimation of neurovasal relations are investigated. Conclusions. The data obtained indicate that intratympanic and suboccipital administration of NEC promotes the regeneration of damaged cell structures of the inner ear. This opens the prospect of using NEC to develop new approaches in the treatment of patients with sensorineural hearing loss.

scholarly journals Antisurdant properties of the structural analogue of taurin

2018 ◽  
Vol 16 (2) ◽  
pp. 25-32
Author(s):  
Lyudmila K Khnychenko ◽  
Natal'ya N Petrova ◽  
Evgeniya V Il'inskaya ◽  
Alexandra E Tanchuk
Keyword(s):  
Clinical Pharmacology ◽  
Hearing Loss ◽  
Drug Therapy ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Guinea Pigs ◽  
Structural Analog ◽  
Sensorineural Hearing ◽  
Structural Analogue ◽  
Nerve Action

The article presents the results of the study of the otoprotective effect of the structural analog of taurine in the case of sensorineural hearing loss. The work was performed on guinea pigs using electrophysiological and cytochemical methods. It is proved that the structural analogue of taurine has an antisurdantant (otoprotective) property, which manifests itself in restoring the amplitude-time characteristics of the potential of the auditory nerve action and the microphone potential of the cochlea. (For citation: Khnychenko LK, Petrova NN, Ilyinskaya EV, Tanchuk AE. Antisurdant properties of the structural analogue of taurin. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(2):25-32. doi: 10.17816/RCF16225-32).

scholarly journals Divergent Auditory Nerve Encoding Deficits Between Two Common Etiologies of Sensorineural Hearing Loss

2019 ◽  
Vol 39 (35) ◽  
pp. 6879-6887 ◽  
Author(s):  
Kenneth S. Henry ◽  
Mark Sayles ◽  
Ann E. Hickox ◽  
Michael G. Heinz
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Sensorineural Hearing

scholarly journals Noise-induced and age-related hearing loss:  new perspectives and potential therapies

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Cell Loss ◽  
Sensorineural Hearing ◽  
Hair Cell Loss ◽  
Age Related ◽  
Age Related Hearing Loss

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.

Exposure of weak magnetic fields on auditory nerve of patients with moderate to severe sensorineural hearing loss

2021 ◽  
Vol 20 (5) ◽  
pp. 63-67
Author(s):  
S. V. Surma ◽  
◽  
D. S. Klyachko ◽  
B. F. Shchegolev ◽  
E. A. Ogorodnikova ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Magnetic Fields ◽  
Sensorineural Hearing Loss ◽  
Hearing Aids ◽  
Auditory Nerve ◽  
Health Hazard ◽  
Sensorineural Deafness ◽  
Pure Tone Audiometry ◽  
Sensorineural Hearing ◽  
Alternative Methods

The article shows that one of the alternative methods of treating moderate to severe sensorineural hearing loss can be the use of an external weak magnetic field. The proposed method is based on the coincidence of the effects caused by the exposure of an external electromagnetic field of certain parameters on the auditory nerve, and natural acoustic exposure. The similarity of reaction allows using of external magnetic fields as an artificial stimulator of the auditory system’s neural part. Induction of applied magnetic fields does not exceed 300 µT, which means that under the current legislation such fields are classified as posing no health hazard. This method was tested at Saint Petersburg Research Institute of Ear, Throat, Nose, and Speech based on relevant Ethics Committee approval and complied with informed consent standards of volunteers. 15 patients aged 18 to 45 with III and IV levels of sensorineural deafness without concomitant pathologies were tested. Threshold pure-tone audiometry was performed on each patient at 500, 1000, 2000, 3000, and 4000 Hz before and after the procedure. The results of the experiments showed that electromagnetic stimulation of auditory neurons allows increasing hearing sensitivity. The proposed procedure may not yield a tangible result in patients with auditory deprivation. Patients with hearing aids showed the most significant results. At the same time, the measurements have shown that the sound thresholds among them became 10 dB lower on the average. The non-invasiveness of the exposure provided additional comfort for the patient.

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.

scholarly journals Enhancing the sensitivity of the envelope-following response for cochlear synaptopathy screening in humans: the role of stimulus envelope

2020 ◽  
Author(s):  
Viacheslav Vasilkov ◽  
Markus Garrett ◽  
Manfred Mauermann ◽  
Sarah Verhulst
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Cell Damage ◽  
Modulation Depth ◽  
Auditory Evoked Potential ◽  
Sensorineural Hearing ◽  
Age Related

AbstractAuditory de-afferentation, a permanent reduction in the number of innerhair-cells and auditory-nerve synapses due to cochlear damage or synaptopathy, can reliably be quantified using temporal bone histology and immunostaining. However, there is an urgent need for non-invasive markers of synaptopathy to study its perceptual consequences in live humans and to develop effective therapeutic interventions. While animal studies have identified candidate auditory-evoked-potential (AEP) markers for synaptopathy, their interpretation in humans has suffered from translational issues related to neural generator differences, unknown hearing-damage histopathologies or lack of measurement sensitivity. To render AEP-based markers of synaptopathy more sensitive and differential to the synaptopathy aspect of sensorineural hearing loss, we followed a combined computational and experimental approach. Starting from the known characteristics of auditory-nerve physiology, we optimized the stimulus envelope to stimulate the available auditory-nerve population optimally and synchronously to generate strong envelope-following-responses (EFRs). We further used model simulations to explore which stimuli evoked a response that was sensitive to synaptopathy, while being maximally insensitive to possible co-existing outer-hair-cell pathologies. We compared the model-predicted trends to AEPs recorded in younger and older listeners (N=44, 24f) who had normal or impaired audiograms with suspected age-related synaptopathy in the older cohort. We conclude that optimal stimulation paradigms for EFR-based quantification of synaptopathy should have sharply rising envelope shapes, a minimal plateau duration of 1.7-2.1 ms for a 120-Hz modulation rate, and inter-peak intervals which contain near-zero amplitudes. From our recordings, the optimal EFR-evoking stimulus had a rectangular envelope shape with a 25% duty cycle and a 95% modulation depth. Older listeners with normal or impaired audiometric thresholds showed significantly reduced EFRs, which were consistent with how (age-induced) synaptopathy affected these responses in the model.Significance StatementCochlear synaptopathy was in 2009 identified as a new form of sensorineural hearing loss (SNHL) that also affects primates and humans. However, clinical practice does not routinely screen for synaptopathy, and hence its consequences for degraded sound and speech perception remain unclear. Cochlear synaptopathy may thus remain undiagnosed and untreated in the aging population who often report self-reported hearing difficulties. To enable an EEG-based differential diagnosis of synaptopathy in humans, it is crucial to develop a recording method that evokes a robust response and emphasizes inter-individual differences. These differences should reflect the synaptopathy aspect of SNHL, while being insensitive to other aspects of SNHL (e.g. outer-hair-cell damage). This study uniquely combines computational modeling with experiments in normal and hearing-impaired listeners to design an EFR stimulation and recording paradigm that can be used for the diagnosis of synaptopathy in humans.

The link between Brain and Hearing system

2020 ◽  
Vol 12 (4) ◽  
pp. 114-117
Author(s):  
Alireza Bina
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Auditory System ◽  
Auditory Nerve ◽  
Neurofibromatosis Type ◽  
Auditory Brainstem ◽  
Auditory Neuropathy ◽  
Sensorineural Hearing ◽  
Brain Disorder ◽  
Hearing System

There are some studies which confirmed that dysfunction in Central Nervous System(CNS) may cause a malfunction in the Peripheral Auditory system (Cochlea_ Auditory Nerve, Auditory Neuropathy), but the question is could Brain Disorder without any lesion in the Cochlea and/or Auditory nerve cause Sensorineural Hearing Loss? It means that the Audiogram shows that the patient suffers from sensorineural hearing loss but the site of the lesion is neither Sensory nor Neural while Brain may be involved in charge of this. And if the answer is yes then could we hear with our Brain and without Cochlea and /or Auditory nerve? We deal with this subject in this paper by: Otosclerosis and Meniere’s disease and The Brain Involvement. Hearing Loss following dysfunction in the Central Auditory and/or central non auditory system. Auditory Brainstem Implant in Patients who suffer from Neurofibromatosis Type two compare to Non Tumor cases, Mondini Syndrome, Michel aplasia. Possible role of Utricle and Saccule in Auditory (Hearing) System We propose a new Hypothesis that the External Ear Canal is not the only input of Auditory Signals, Sounds could transfer by our eyes and skin to the Cerebral Cortex and approach to the Cochlea (Backward Auditory input pathway of Sounds).

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