Mechanism of Efferent Inhibition in Cochlear Hair Cell

2013 ◽  
Vol 56 (2) ◽  
pp. 61
Author(s):  
Gi Jung Im
Keyword(s):  
Hair Cell ◽  
Cochlear Hair Cell ◽  
Efferent Inhibition

Histological evaluation of cochlear hair cell damage from noise-induced hearing loss in chinchillas

1990 ◽  
Vol 48 (3) ◽  
pp. 332-333
Author(s):  
R.V. Harrison ◽  
R.J. Mount ◽  
P. White ◽  
N. Fukushima
Keyword(s):  
Hair Cell ◽  
Evoked Potential ◽  
Cell Damage ◽  
Acoustic Trauma ◽  
Histological Evaluation ◽  
Cell Integrity ◽  
Functional Changes ◽  
Cochlear Hair Cell ◽  
Left And Right ◽  
Contralateral Ear

In studies which attempt to define the influence of various factors on recovery of hair cell integrity after acoustic trauma, an experimental and a control ear which initially have equal degrees of damage are required. With in a group of animals receiving an identical level of acoustic trauma there is more symmetry between the ears of each individual, in respect to function, than between animals. Figure 1 illustrates this, left and right cochlear evoked potential (CAP) audiograms are shown for two chinchillas receiving identical trauma. For this reason the contralateral ear is used as control.To compliment such functional evaluations we have devised a scoring system, based on the condition of hair cell stereocilia as revealed by scanning electron microscopy, which permits total stereociliar damage to be expressed numerically. This quantification permits correlation of the degree of structural pathology with functional changes. In this paper wereport experiments to verify the symmetry of stereociliar integrity between two ears, both for normal (non-exposed) animals and chinchillas in which each ear has received identical noise trauma.

scholarly journals Ceramide/sphingomyelin cycle involvement in gentamicin-induced cochlear hair cell death

2014 ◽  
Vol 89 (3) ◽  
pp. 415-421 ◽  
Author(s):  
Le Nguyen Uyen Chi ◽  
Keiji Tabuchi ◽  
Mariko Nakamagoe ◽  
Masahiro Nakayama ◽  
Bungo Nishimura ◽  
...  
Keyword(s):  
Cell Death ◽  
Hair Cell ◽  
Cochlear Hair Cell ◽  
Hair Cell Death ◽  
Sphingomyelin Cycle

scholarly journals Effects of cochlear hair cell ablation on spatial learning/memory

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Z. Jason Qian ◽  
Anthony J. Ricci
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Spatial Learning ◽  
Hair Cells ◽  
Noise Exposure ◽  
Memory Errors ◽  
Cochlear Hair Cells ◽  
Cochlear Hair Cell ◽  
Cell Ablation ◽  
Spatial Learning Memory

AbstractCurrent clinical interest lies in the relationship between hearing loss and cognitive impairment. Previous work demonstrated that noise exposure, a common cause of sensorineural hearing loss (SNHL), leads to cognitive impairments in mice. However, in noise-induced models, it is difficult to distinguish the effects of noise trauma from subsequent SNHL on central processes. Here, we use cochlear hair cell ablation to isolate the effects of SNHL. Cochlear hair cells were conditionally and selectively ablated in mature, transgenic mice where the human diphtheria toxin (DT) receptor was expressed behind the hair-cell specific Pou4f3 promoter. Due to higher Pou4f3 expression in cochlear hair cells than vestibular hair cells, administration of a low dose of DT caused profound SNHL without vestibular dysfunction and had no effect on wild-type (WT) littermates. Spatial learning/memory was assayed using an automated radial 8-arm maze (RAM), where mice were trained to find food rewards over a 14-day period. The number of working memory errors (WME) and reference memory errors (RME) per training day were recorded. All animals were injected with DT during P30–60 and underwent the RAM assay during P90–120. SNHL animals committed more WME and RME than WT animals, demonstrating that isolated SNHL affected cognitive function. Duration of SNHL (60 versus 90 days post DT injection) had no effect on RAM performance. However, younger age of acquired SNHL (DT on P30 versus P60) was associated with fewer WME. This describes the previously undocumented effect of isolated SNHL on cognitive processes that do not directly rely on auditory sensory input.

Hearing Preservation After Translabyrinthine Vestibular Schwannoma Excision: Audiometry and Electrocochleography Results

2018 ◽  
Vol 127 (8) ◽  
pp. 563-567 ◽  
Author(s):  
Kenneth Akakpo ◽  
William J. Riggs ◽  
Michael S. Harris ◽  
Edward E Dodson
Keyword(s):  
Hair Cell ◽  
Vestibular Schwannoma ◽  
Cranial Nerve ◽  
Cell Activity ◽  
Internal Auditory Canal ◽  
Hearing Preservation ◽  
Healthy Patient ◽  
Cochlear Hair Cell ◽  
Translabyrinthine Approach ◽  
Cranial Nerve Viii

Objectives: To describe a case of inadvertent hearing preservation following a classical translabyrinthine resection of a vestibular schwannoma of the internal auditory canal in an otherwise healthy patient. Methods: Herein, we describe the case of an otherwise healthy patient who underwent resection of an intracanalicular vestibular schwannoma via a translabyrinthine approach. Furthermore, as part of an ongoing study aimed at characterizing hearing changes due to intraoperative events, cochlear hair cell and nerve activity were monitored using electrocochleography throughout surgery. Unexpectedly, the patient maintained serviceable hearing following surgery. As a result, we are able to provide electrophysiologic evidence of cochlear hair cell activity at various stages of this surgery. Results: Hair cell responses across tested frequencies were detectable prior to and following completion of the translabyrinthine procedure. Neural integrity of the auditory division of cranial nerve VIII was maintained throughout. Lastly, postoperative audiometric testing supported the patient’s subjective assertion of serviceable hearing in the surgical ear. Conclusion: Our results suggest that some degree of hair cell and neural integrity can be maintained throughout the course of the translabyrinthine approach, and if preservation of the auditory division of cranial nerve VIII is feasible, a functional amount of hearing preservation is attainable.

Protective Effect of Ginsenoside Rd on Military Aviation Noise-Induced Cochlear Hair Cell Damage

2021 ◽  
Author(s):  
Xuemin Chen ◽  
Yu-hui LIU ◽  
Shuai-fei JI ◽  
Xin-miao XUE ◽  
Peng LIU ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hair Cell ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Outer Hair Cells ◽  
Ginsenoside Rd ◽  
Cochlear Hair Cell ◽  
Aviation Noise ◽  
Military Aviation ◽  
Hair Cell Damage

Abstract Background Soldiers are often exposed to high-intensity noise produced by military weapons and equipment during activities, and the incidence of noise-induced hearing loss (NIHL) in many arms is high. Oxidative stress has a significant role in the pathogenesis of NIHL, and research has confirmed that ginsenoside Rd (GSRd) suppresses oxidative stress. Therefore, we hypothesized that GSRd may attenuate NIHL and cochlear hair cell loss, induced by military aviation noise stimulation, through the Sirtuin1/proliferator-activated receptor-gamma coactivator 1α (SIRT1/PGC-1α) signaling pathway.Methods Forty-eight male guinea pigs were randomly divided into four groups: control, noise stimulation, GSRd, and glycerol. The experimental groups received military helicopter noise stimulation at 115 dB (A) for 4 h daily for five consecutive days. Hair cell damage was evaluated by using inner ear basilar membrane preparation and scanning electron microscopy. Terminal dUTP nick end labeling and immunofluorescence staining were conducted. Changes in the SIRT1/PGC-1α signaling pathway and other apoptosis-related markers in the cochleae, as well as oxidative stress parameters were used as readouts.Results Loss of outer hair cells, more disordered cilia, prominent apoptosis, and elevated free radical levels were observed in the experimental groups. GSRd treatment markedly improved morphological changes and apoptosis through decreasing Bcl-2 associated X protein (Bax) expression and increasing Bcl-2 expression. In addition, GSRd upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels, decreased malondialdehyde (MDA) levels, and enhanced the activity of SIRT1 and PGC-1α messenger ribonucleic acid and protein expression.Conclusion GSRd can improve structural and functional damage to the cochleae caused by noise. The underlying mechanisms may be associated with the SIRT1/PGC-1α signaling pathway.

Shaker-1 mutations reveal roles for myosin VIIA in both development and function of cochlear hair cells

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 557-566 ◽  
Author(s):  
T. Self ◽  
M. Mahony ◽  
J. Fleming ◽  
J. Walsh ◽  
S.D. Brown ◽  
...  
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Usher Syndrome ◽  
Orthologous Gene ◽  
Cell Development ◽  
Cochlear Hair Cells ◽  
Cochlear Hair Cell ◽  
Show Evidence ◽  
Myosin Viia ◽  
And Function

The mouse shaker-1 locus, Myo7a, encodes myosin VIIA and mutations in the orthologous gene in humans cause Usher syndrome type 1B or non-syndromic deafness. Myo7a is expressed very early in sensory hair cell development in the inner ear. We describe the effects of three mutations on cochlear hair cell development and function. In the Myo7a816SB and Myo7a6J mutants, stereocilia grow and form rows of graded heights as normal, but the bundles become progressively more disorganised. Most of these mutants show no gross electrophysiological responses, but some did show evidence of hair cell depolarisation despite the disorganisation of their bundles. In contrast, the original shaker-1 mutants, Myo7ash1, had normal early development of stereocilia bundles, but still showed abnormal cochlear responses. These findings suggest that myosin VIIA is required for normal stereocilia bundle organisation and has a role in the function of cochlear hair cells.

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