Estimation of surviving spiral ganglion cells in the deaf rat using the electrically evoked auditory brainstem response

1990 ◽  
Vol 49 (1-3) ◽  
pp. 155-168 ◽  
Author(s):  
Robert D Hall
2021 ◽  
Author(s):  
Yazhi Xing ◽  
Jia Fang ◽  
Zhuangzhuang Li ◽  
Mingxian Li ◽  
Chengqi Liu ◽  
...  

Abstract Background In aminoglycoside-induced hearing loss, damage to spiral ganglion neurons (SGNs) accelerates gradually after the acute outer hair cell death, accompanied by macrophage infiltration and cytokine release. Pyroptosis plays a critical role in neurodegenerative diseases. Here, we explored the potential role of pyroptosis in SGN degeneration. Methods C57BL/6J mice were randomly divided into a kanamycin plus furosemide group and saline control group. Auditory functions were evaluated by auditory brainstem response tests conducted before treatment and at 1, 5, 15, and 30 days after treatment. HCs and SGNs were assessed for morphological alterations. SGNs were subjected to RNA sequencing and mRNA and protein analyses of NLRP3 inflammasome-related molecules. Macrophage activation was evaluated based on morphological and mRNA alterations. The effect of NLRP3 inhibition on SGN survival after kanamycin treatment was evaluated in organ explant cultures treated with Mcc950, a specific inhibitor of the NLRP3 inflammasome. Results Kanamycin and furosemide administration led to irreversible deterioration of the auditory brainstem response threshold, accompanied by acute loss of outer hair cells and gradually progressive loss of inner hair cells. SGNs showed a progressive decrease in quantity, as well as swelling and membrane rupture, at 15 and 30 days. RNA sequencing of SGNs showed that inflammation and immune-related responses were significantly upregulated, as was the expression of the inflammasome-related gene NLRP3. During 30 days of kanamycin exposure, the canonical pyroptosis pathway was constantly activated in SGNs. Activation and infiltration of microglia-like cells/macrophages, and increased production of cytokines, hallmarks of neuroinflammation, were also observed. Mcc950 significantly ameliorated SGN degeneration by inhibiting NLRP3 expression and promoting release of interleukins 1β and 18. Conclusions Pyroptosis causes cell death during aminoglycoside-induced SGN degeneration. Activation of the NLRP3 inflammasome leads to a cascade of inflammatory events in SGNs. Inhibition of the NLRP3 inflammasome significantly alleviates SGN damage, suggesting that it could serve as a new molecular target for the treatment of aminoglycoside-induced SGN degeneration.


1984 ◽  
Vol 93 (4_suppl) ◽  
pp. 97-100 ◽  
Author(s):  
F. Blair Simmons ◽  
Tom Meyers ◽  
Hugh S. Lusted ◽  
Clough Shelton

Nerve survival estimates in totally deaf ears of cats and humans can be easily obtained by auditory brainstem responses to electrical stimulation at the round window. In humans, electrically induced auditory brainstem responses require considerably more current than concurrently observed perceptual thresholds and “maximum loudnesses,” and there is much variability from patient to patient. In cats, in which we also compared efficacy of stimulation sites, preliminary data analysis suggests that the scala tympani is clearly much more efficient than the round window, and the round window better than the promontory in ears with large populations of ganglion cells. In ears with no or nearly no ganglion cells, scala tympani and round window stimulations are about equal.


2010 ◽  
Vol 125 (5) ◽  
pp. 449-454 ◽  
Author(s):  
S-Q Zhai ◽  
W Guo ◽  
Y-Y Hu ◽  
N Yu ◽  
Q Chen ◽  
...  

AbstractObjective:To explore the protective effects of brain-derived neurotrophic factor on the noise-damaged cochlear spiral ganglion.Methods:Recombinant adenovirus brain-derived neurotrophic factor vector, recombinant adenovirus LacZ and artificial perilymph were prepared. Guinea pigs with audiometric auditory brainstem response thresholds of more than 75 dB SPL, measured seven days after four hours of noise exposure at 135 dB SPL, were divided into three groups. Adenovirus brain-derived neurotrophic factor vector, adenovirus LacZ and perilymph were infused into the cochleae of the three groups, variously. Eight weeks later, the cochleae were stained immunohistochemically and the spiral ganglion cells counted.Results:The auditory brainstem response threshold recorded before and seven days after noise exposure did not differ significantly between the three groups. However, eight weeks after cochlear perfusion, the group receiving brain-derived neurotrophic factor had a significantly decreased auditory brainstem response threshold and increased spiral ganglion cell count, compared with the adenovirus LacZ and perilymph groups.Conclusion:When administered via cochlear infusion following noise damage, brain-derived neurotrophic factor appears to improve the auditory threshold, and to have a protective effect on the spiral ganglion cells.


1983 ◽  
Vol 92 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Lee Smith ◽  
F. Blair Simmons

Determining nerve survival is important in selecting patients for cochlear implants, and in predicting outcomes from such implants. In search of a possible method we deliberately destroyed nerve fibers (ganglion cells) in 17 cat cochleas to produce a range of degenerations Months later, we electrically stimulated these ears (and seven controls) and recorded electrical ABR input-output functions. Cats with no surviving ganglion cells showed no ABR activity. Cats with 5%–10% surviving cells had ABRs which typically had normal thresholds but decreased input-output functions. The suprathreshold slopes of these input-output functions reliably predicted ganglion cell survival for all degrees of degeneration. Thus perceptual (or electrical) threshold is a poor indicator of nerve survival. Loudness growth (or growth in the electrically-induced auditory brainstem response) is a good index of surviving ganglion cells.


2012 ◽  
Vol 126 (11) ◽  
pp. 1091-1096 ◽  
Author(s):  
M Topdag ◽  
M Iseri ◽  
E Gelenli ◽  
M Yardimoglu ◽  
Y Yazir ◽  
...  

AbstractObjective:This study aimed to contribute to the literature on the prevention and treatment of ototoxicity due to various drugs and chemicals.Material and methods:This study compared the histological effects of intratympanic dexamethasone, memantine and piracetam on cellular apoptosis due to cisplatin ototoxicity, in 36 rats.Results:Dexamethasone and memantine had significant effects on the stria vascularis, organ of Corti and spiral ganglion (p < 0.05). Although piracetam decreased the apoptosis rate, this effect was not statistically significant (p > 0.05).Conclusion:Dexamethasone and memantine were found superior to piracetam in reducing apoptosis due to cisplatin ototoxicity. Further studies of this subject are needed, incorporating electron microscopy and auditory brainstem response testing.


2011 ◽  
Vol 125 (9) ◽  
pp. 917-923 ◽  
Author(s):  
F Wang ◽  
X Gao ◽  
J Chen ◽  
S-L Liu ◽  
F-Y Wang ◽  
...  

AbstractObjective:To evaluate the effect of early postnatal air-conduction auditory deprivation on the development and function of the rat spiral ganglion.Study design:Randomised animal study.Methods:Sixty neonatal Sprague–Dawley rats were randomly divided into two groups: controls (n = 30) given regular chow and water ad libitum; and study animals (n = 30) fed within a soundproof chamber. Auditory brainstem response testing was conducted in both groups on postnatal day 42.Results:Auditory deprivation between postnatal days 12 and 42 resulted in an increased hearing threshold and reduced auditory brainstem response amplitudes, together with degeneration of type I spiral ganglion neurons and the presence of apoptotic cells.Conclusion:Non-invasive auditory deprivation during a critical developmental period resulted in numerous changes in rat cochlear function and morphology.


2010 ◽  
Author(s):  
Sara C. Therrien ◽  
Catherine E. Carr ◽  
Elizabeth F. Brittan-Powell ◽  
Alicia M. Wells-Berlin

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