scholarly journals Peak I of the human auditory brainstem response results from the somatic regions of type I spiral ganglion cells: Evidence from computer modeling

2014 ◽  
Vol 315 ◽  
pp. 67-79 ◽  
Author(s):  
Frank Rattay ◽  
Simon M. Danner
Keyword(s):  
Computer Modeling ◽  
Auditory Brainstem Response ◽  
Ganglion Cells ◽  
Spiral Ganglion ◽  
Auditory Brainstem ◽  
Type I ◽  
Brainstem Response

Effect of early postnatal air-conduction auditory deprivation on the development and function of the rat spiral ganglion

2011 ◽  
Vol 125 (9) ◽  
pp. 917-923 ◽  
Author(s):  
F Wang ◽  
X Gao ◽  
J Chen ◽  
S-L Liu ◽  
F-Y Wang ◽  
...  
Keyword(s):  
Auditory Brainstem Response ◽  
Spiral Ganglion ◽  
Auditory Brainstem ◽  
Type I ◽  
Cochlear Function ◽  
Auditory Deprivation ◽  
Brainstem Response ◽  
Ganglion Neurons ◽  
And Function ◽  
Air Conduction

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.

scholarly journals Pyroptosis Accelerates Spiral Ganglion Neuronal Degeneration Induced by Aminoglycosides in the Cochlea

2021 ◽  
Author(s):  
Yazhi Xing ◽  
Jia Fang ◽  
Zhuangzhuang Li ◽  
Mingxian Li ◽  
Chengqi Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Rna Sequencing ◽  
Hair Cells ◽  
Nlrp3 Inflammasome ◽  
Auditory Brainstem Response ◽  
Spiral Ganglion ◽  
Auditory Brainstem ◽  
Response Threshold ◽  
Brainstem Response ◽  
Ganglion Neurons

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.

Diffusion Tensor Imaging of Auditory Pathway in Patients With Crigler-Najjar Syndrome Type I: Correlation With Auditory Brainstem Response

2021 ◽  
pp. 088307382110258
Author(s):  
Ahmed Abdel Khalek Abdel Razek ◽  
Mohamed Ezz El Regal ◽  
Mortada El-Shabrawi ◽  
Mohamed Moustafa Abdeltawwab ◽  
Ahmed Megahed ◽  
...  
Keyword(s):  
Diffusion Tensor Imaging ◽  
Inferior Colliculus ◽  
Cochlear Nucleus ◽  
Auditory Brainstem Response ◽  
Diffusion Tensor ◽  
Auditory Brainstem ◽  
Type I ◽  
Syndrome Type ◽  
Brainstem Response ◽  
Olivary Nucleus

Aim: To evaluate the role of diffusion tensor imaging of the auditory pathway in patients with Crigler Najjar syndrome type I and its relation to auditory brainstem response. Methods: Prospective study was done including 12 patients with Crigler Najjar syndrome type I and 10 age- and sex-matched controls that underwent diffusion tensor imaging of brain. Mean diffusivity and fractional anisotropy at 4 regions of the brain and brainstem on each side were measured and correlated with the results of auditory brainstem response for patients. Results: There was significantly higher mean diffusivity of cochlear nucleus, superior olivary nucleus, inferior colliculus, and auditory cortex of patients versus controls on both sides for all regions ( P = .001). The fractional anisotropy of cochlear nucleus, superior olivary nucleus, inferior colliculus, and auditory cortex of patients versus controls was significantly lower, with P values of, respectively, .001, .001, .003, and .001 on the right side and .001, .001, .003, and .001 on left side, respectively. Also, a negative correlation was found between the maximum bilirubin level and fractional anisotropy of the left superior olivary nucleus and inferior colliculus of both sides. A positive correlation was found between the mean diffusivity and auditory brainstem response wave latency of the right inferior colliculus and left cochlear nucleus. The fractional anisotropy and auditory brainstem response wave latency of the right superior olivary nucleus, left cochlear nucleus, and inferior colliculus of both sides were negatively correlated. Conclusion: Diffusion tensor imaging can detect microstructural changes in the auditory pathway in Crigler Najjar syndrome type I that can be correlated with auditory brainstem response.

Thalamocortical abnormalities in auditory brainstem response patterns distinguish DSM-IV bipolar disorder type I from schizophrenia

2014 ◽  
Vol 169 ◽  
pp. 105-111 ◽  
Author(s):  
Mia Sköld ◽  
Johan Källstrand ◽  
Sara Nehlstedt ◽  
Annelie Nordin ◽  
Sören Nielzén ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Auditory Brainstem Response ◽  
Auditory Brainstem ◽  
Type I ◽  
Response Patterns ◽  
Brainstem Response ◽  
Dsm Iv ◽  
Disorder Type

scholarly journals Contralateral Suppression of DPOAEs in Mice after Ouabain Treatment

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jieying Li ◽  
Yan Chen ◽  
Shan Zeng ◽  
Chuijin Lai ◽  
Yanping Zhang ◽  
...  
Keyword(s):  
Otoacoustic Emissions ◽  
Round Window ◽  
Spiral Ganglion ◽  
Auditory Brainstem ◽  
Spiral Ganglion Neurons ◽  
Type I ◽  
Type Ii ◽  
Contralateral Suppression ◽  
Brainstem Response ◽  
Ganglion Neurons

Medial olivocochlear (MOC) efferent feedback is suggested to protect the ear from acoustic injury and to increase its ability to discriminate sounds against a noisy background. We investigated whether type II spiral ganglion neurons participate in the contralateral suppression of the MOC reflex. The application of ouabain to the round window of the mouse cochlea selectively induced the apoptosis of the type I spiral ganglion neurons, left the peripherin-immunopositive type II spiral ganglion neurons intact, and did not affect outer hairs, as evidenced by the maintenance of the distorted product otoacoustic emissions (DPOAEs). With the ouabain treatment, the threshold of the auditory brainstem response increased significantly and the amplitude of wave I decreased significantly in the ouabain-treated ears, consistent with the loss of type I neurons. Contralateral suppression was measured as reduction in the amplitude of the 2f1−f2 DPOAEs when noise was presented to the opposite ear. Despite the loss of all the type I spiral ganglion neurons, virtually, the amplitude of the contralateral suppression was not significantly different from the control when the suppressor noise was delivered to the treated cochlea. These results are consistent with the type II spiral ganglion neurons providing the sensory input driving contralateral suppression of the MOC reflex.

Electrically Induced Auditory Brainstem Response as a Clinical Tool in Estimating Nerve Survival

1984 ◽  
Vol 93 (4_suppl) ◽  
pp. 97-100 ◽  
Author(s):  
F. Blair Simmons ◽  
Tom Meyers ◽  
Hugh S. Lusted ◽  
Clough Shelton
Keyword(s):  
Auditory Brainstem Response ◽  
Ganglion Cells ◽  
Round Window ◽  
Auditory Brainstem ◽  
Auditory Brainstem Responses ◽  
Scala Tympani ◽  
Clinical Tool ◽  
Large Populations ◽  
Brainstem Response ◽  
Better Than

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.

Protective effects of brain-derived neurotrophic factor on the noise-damaged cochlear spiral ganglion

2010 ◽  
Vol 125 (5) ◽  
pp. 449-454 ◽  
Author(s):  
S-Q Zhai ◽  
W Guo ◽  
Y-Y Hu ◽  
N Yu ◽  
Q Chen ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Auditory Brainstem Response ◽  
Noise Exposure ◽  
Recombinant Adenovirus ◽  
Spiral Ganglion ◽  
Brain Derived Neurotrophic Factor ◽  
Auditory Brainstem ◽  
Response Threshold ◽  
Protective Effects ◽  
Brainstem Response

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.

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