scholarly journals Neuroprotective Effect of Near-Infrared Light in an Animal Model of CI Surgery

2020 ◽  
pp. 1-7
Author(s):  
Ira Strübing ◽  
Moritz Gröschel ◽  
Susanne Schwitzer ◽  
Arne Ernst ◽  
Felix Fröhlich ◽  
...  
Keyword(s):  
Animal Model ◽  
Hearing Loss ◽  
Hair Cells ◽  
Cochlear Implantation ◽  
Near Infrared ◽  
Outer Hair Cells ◽  
Auditory Brainstem Responses ◽  
Infrared Light ◽  
Residual Hearing ◽  
Significant Difference

<b><i>Introduction:</i></b> The preservation of residual hearing has become an important consideration in cochlear implant (CI) recipients in recent years. It was the aim of the present animal experimental study to investigate the influence of a pretreatment with near-infrared (NIR) light on preservation of sensory hair cells and residual hearing after cochlear implantation. <b><i>Methods:</i></b> NIR was applied unilaterally (15 min, 808 nm, 120 mW) to 8 guinea pigs, immediately before a bilateral scala tympani CI electrode insertion was performed. The nonirradiated (contralateral) side served as control. Twenty-eight days postoperatively, auditory brainstem responses (ABRs) were registered from both ears to screen for hearing loss. Thereafter, the animals were sacrificed and inner hair cells (IHCs) and outer hair cells (OHCs) were counted and compared between NIR-pretreated and control (contralateral) cochleae. <b><i>Results:</i></b> There was no IHC loss upon cochlear implantation. OHC loss was most prominent on both sides at the apical part of the cochlea. NIR pretreatment led to a statistically significant reduction in OHC loss (by 39.8%). ABR recordings (across the frequencies 4–32 kHz) showed a statistically significant difference between the 2 groups and corresponds well with the apical structural damage. Hearing loss was reduced by about 20 dB on average for the NIR-pretreated group (<i>p</i> ≤ 0.05). <b><i>Discussion/Conclusion:</i></b> A single NIR pretreatment in this animal model of CI surgery appears to be neuroprotective for residual hearing. This is in line with other studies where several NIR posttreatments have protected cochlear and other neural tissues. NIR pretreatment is an inexpensive, effective, and noninvasive approach that can complement other ways of preserving residual hearing and, hence, should deserve further clinical evaluation in CI patients.

scholarly journals miR-153/KCNQ4 axis contributes to noise-induced hearing loss in a mouse model

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Qin Wang ◽  
Wei Li ◽  
Cuiyun Cai ◽  
Peng Hu ◽  
Ruosha Lai
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Sensory Epithelium ◽  
Outer Hair Cells ◽  
Broadband Noise ◽  
Hek293 Cells ◽  
Auditory Brainstem Responses ◽  
Luciferase Reporter

AbstractDamage to the cochlear sensory epithelium is a key contributor to noise-induced sensorineural hearing loss (SNHL). KCNQ4 plays an important role in the cochlear potassium circulation and outer hair cells survival. As miR-153 can target and regulate KCNQ4, we sought to study the role of miR-153 in SNHL. 12-week-old male CBA/J mice were exposed to 2–20 kHz broadband noise at 96 dB SPL to induce temporary threshold shifts and 101 dB SPL to induce permanent threshold shifts. Hearing loss was determined by auditory brainstem responses (ABR). Relative expression of miR-153 and KCNQ4 in mice cochlea were determined by Real-Time quantitative PCR. miR-153 mimics were co-transfected with wild type or mutated KCNQ4 into HEK293 cells. Luciferase reporter assay was used to validate the binding between miR-153 and KCNQ4. AAV-sp-153 was constructed and administrated intra-peritoneally 24- and 2-h prior and immediately after noise exposure to knockdown miR-153. The KCNQ4 is mainly expressed in outer hair cells (OHCs). We showed that the expression of KCNQ4 in mice cochlea was reduced and miR-153 expression was significantly increased after noise exposure compared to control. miR-153 bound to 3′UTR of KNCQ4, and the knockdown of miR-153 with the AAV-sp-153 administration restored KCNQ4 mRNA and protein expression. In addition, the knockdown of miR-153 reduced ABR threshold shifts at 8, 16, and 32 kHz after permanent threshold shifts (PTS) noise exposure. Correspondingly, OHC losses were attenuated with inhibition of miR-153. This study demonstrates that miR-153 inhibition significantly restores KNCQ4 in cochlea after noise exposure, which attenuates SNHL. Our study provides a new potential therapeutic target in the prevention and treatment of SNHL.

Delaying Cochlear Implantation Impacts Postoperative Speech Perception of Nontraditional Pediatric Candidates

2020 ◽  
pp. 1-6
Author(s):  
Lisa R. Park ◽  
Elizabeth L. Perkins ◽  
Jennifer S. Woodard ◽  
Kevin D. Brown
Keyword(s):  
Hearing Loss ◽  
Speech Perception ◽  
Word Recognition ◽  
Cochlear Implantation ◽  
Delay Time ◽  
Residual Hearing ◽  
Progressive Hearing Loss ◽  
Significant Difference ◽  
Significant Regression ◽  
The Impact

<b><i>Introduction:</i></b> As pediatric cochlear implant (CI) candidacy expands, children with greater degrees of residual hearing are receiving CIs. These nontraditional candidates have audiometric thresholds that meet adult manufacturer labeling but are better than current pediatric guidelines allow. The purpose of this study was to determine the impact of delayed cochlear implantation on speech perception in nontraditional pediatric CI recipients. <b><i>Methods:</i></b> Pediatric CI recipients with a history of progressive hearing loss and a preoperative 4-frequency pure-tone average of ≤75 dB HL at the time of implantation were considered for this retrospective study. Preoperative serial audiograms and word recognition scores were reviewed, and a method was created to establish a date when each individual ear 1st met nontraditional candidacy. The length of time between the date of candidacy and implantation was calculated and defined as the “delay time.” A multiple linear regression investigated delay time, age at surgery, surgery type (1st vs. 2nd side), and array type as predictive factors of maximum postoperative Consonant-Nucleus-Consonant (CNC) word scores. A one-way ANCOVA was performed comparing the postoperative CNC scores between subjects grouped by delay time. <b><i>Results:</i></b> A significant regression was found (<i>F</i>(4, 38) = 5.167, <i>p</i> = 0.002, <i>R</i><sup>2</sup> = 0.353). Both age at implantation (<i>p</i> = 0.023) and delay time (<i>p</i> = 0.002) predicted CNC word scores. Longer delay time was associated with poorer word recognition scores, while older age at implantation correlated with higher CNC word scores in this progressive hearing loss group. A significant difference was noted between subjects implanted with &#x3c;1 year of delay and those with 3 or more years of delay (<i>p</i> = 0.003). All ears implanted within a year of candidacy achieved word recognition abilities that are generally accepted as above average (<i>M</i> = 84.91). <b><i>Conclusion:</i></b> CI candidacy for adults has evolved to allow for greater degrees of residual hearing, while audiometric guidelines for children have not changed since 2000. Our findings suggest that delay of cochlear implantation, even for children with significant levels of residual hearing, leads to poorer outcomes. Modified candidacy guidelines for children should be established to expedite referral to multidisciplinary CI teams and minimize delays in this population.

scholarly journals Preventing presbycusis in mice with enhanced medial olivocochlear feedback

2020 ◽  
Vol 117 (21) ◽  
pp. 11811-11819 ◽  
Author(s):  
Luis E. Boero ◽  
Valeria C. Castagna ◽  
Gonzalo Terreros ◽  
Marcelo J. Moglie ◽  
Sebastián Silva ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Outer Hair Cells ◽  
Auditory Brainstem Responses ◽  
Cochlear Function ◽  
Gain Of Function ◽  
Distortion Product ◽  
Age Related ◽  
Medial Olivocochlear ◽  
Age Related Hearing Loss

“Growing old” is the most common cause of hearing loss. Age-related hearing loss (ARHL) (presbycusis) first affects the ability to understand speech in background noise, even when auditory thresholds in quiet are normal. It has been suggested that cochlear denervation (“synaptopathy”) is an early contributor to age-related auditory decline. In the present work, we characterized age-related cochlear synaptic degeneration and hair cell loss in mice with enhanced α9α10 cholinergic nicotinic receptors gating kinetics (“gain of function” nAChRs). These mediate inhibitory olivocochlear feedback through the activation of associated calcium-gated potassium channels. Cochlear function was assessed via distortion product otoacoustic emissions and auditory brainstem responses. Cochlear structure was characterized in immunolabeled organ of Corti whole mounts using confocal microscopy to quantify hair cells, auditory neurons, presynaptic ribbons, and postsynaptic glutamate receptors. Aged wild-type mice had elevated acoustic thresholds and synaptic loss. Afferent synapses were lost from inner hair cells throughout the aged cochlea, together with some loss of outer hair cells. In contrast, cochlear structure and function were preserved in aged mice with gain-of-function nAChRs that provide enhanced olivocochlear inhibition, suggesting that efferent feedback is important for long-term maintenance of inner ear function. Our work provides evidence that olivocochlear-mediated resistance to presbycusis-ARHL occurs via the α9α10 nAChR complexes on outer hair cells. Thus, enhancement of the medial olivocochlear system could be a viable strategy to prevent age-related hearing loss.

scholarly journals Near-infrared-light pre-treatment attenuates noise-induced hearing loss in mice

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9384
Author(s):  
Dietmar Basta ◽  
Moritz Gröschel ◽  
Ira Strübing ◽  
Patrick Boyle ◽  
Felix Fröhlich ◽  
...  
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Near Infrared ◽  
Noise Exposure ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Infrared Light ◽  
Hair Cell Loss ◽  
Nir Light ◽  
Pre Treatment

Noise induced hearing loss (NIHL) is accompanied by a reduction of cochlear hair cells and spiral ganglion neurons. Different approaches have been applied to prevent noise induced apoptosis / necrosis. Physical intervention is one technique currently under investigation. Specific wavelengths within the near-infrared light (NIR)-spectrum are known to influence cytochrome-c-oxidase activity, which leads in turn to a decrease in apoptotic mechanisms. It has been shown recently that NIR can significantly decrease the cochlear hair cell loss if applied daily for 12 days after a noise exposure. However, it is still unclear if a single NIR-treatment, just before a noise exposure, could induce similar protective effects. Therefore, the present study was conducted to investigate the effect of a single NIR-pre-treatment aimed at preventing or limiting NIHL. The cochleae of adult NMRI-mice were pre-treated with NIR-light (808 nm, 120 mW) for 5, 10, 20, 30 or 40 minutes via the external ear canal. All animals were noised exposed immediately after the pre-treatment by broad band noise (5–20 kHz) for 30 minutes at 115 dB SPL. Frequency specific ABR-recordings to determine auditory threshold shift were carried out before the pre-treatment and two weeks after the noise exposure. The amplitude increase for wave IV and cochlear hair cell loss were determined. A further group of similar mice was noise exposed only and served as a control for the NIR pre-exposed groups. Two weeks after noise exposure, the ABR threshold shifts of NIR-treated animals were significantly lower (p < 0.05) than those of the control animals. The significance was at three frequencies for the 5-minute pre-treatment group and across the entire frequency range for all other treatment groups. Due to NIR light, the amplitude of wave four deteriorates significantly less after noise exposure than in controls. The NIR pre-treatment had no effect on the loss of outer hair cells, which was just as high with or without NIR-light pre-exposure. Relative to the entire number of outer hair cells across the whole cochlea, outer hair cell loss was rather negligible. No inner hair cell loss whatever was detected. Our results suggest that a single NIR pre-treatment induces a very effective protection of cochlear structures from noise exposure. Pre-exposure of 10 min seems to emerge as the optimal dosage for our experimental setup. A saturated effect occurred with higher dosage-treatments. These results are relevant for protection of residual hearing in otoneurosurgery such as cochlear implantation.

scholarly journals Effect of shock wave power spectrum on the inner ear pathophysiology in blast-induced hearing loss

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eiko Kimura ◽  
Kunio Mizutari ◽  
Takaomi Kurioka ◽  
Satoko Kawauchi ◽  
Yasushi Satoh ◽  
...  
Keyword(s):  
Shock Wave ◽  
Hearing Loss ◽  
Power Spectrum ◽  
Hair Cells ◽  
High Frequency ◽  
Low Frequency ◽  
Outer Hair Cells ◽  
Auditory Brainstem Responses ◽  
Pathological Examination ◽  
Blast Exposure

AbstractBlast exposure can induce various types of hearing impairment, including permanent hearing loss, tinnitus, and hyperacusis. Herein, we conducted a detailed investigation of the cochlear pathophysiology in blast-induced hearing loss in mice using two blasts with different characteristics: a low-frequency dominant blast generated by a shock tube and a high-frequency dominant shock wave generated by laser irradiation (laser-induced shock wave). The pattern of sensorineural hearing loss (SNHL) was low-frequency- and high-frequency-dominant in response to the low- and high-frequency blasts, respectively. Pathological examination revealed that cochlear synaptopathy was the most frequent cochlear pathology after blast exposure, which involved synapse loss in the inner hair cells without hair cell loss, depending on the power spectrum of the blast. This pathological change completely reflected the physiological analysis of wave I amplitude using auditory brainstem responses. Stereociliary bundle disruption in the outer hair cells was also dependent on the blast’s power spectrum. Therefore, we demonstrated that the dominant frequency of the blast power spectrum was the principal factor determining the region of cochlear damage. We believe that the presenting models would be valuable both in blast research and the investigation of various types of hearing loss whose pathogenesis involves cochlear synaptopathy.

Impact of Cochlear Implantation on Neurocognitive Subdomains in Adult Cochlear Implant Recipients

2021 ◽  
pp. 1-10
Author(s):  
Christiane Völter ◽  
Lisa Götze ◽  
Imme Haubitz ◽  
Janine Müther ◽  
Stefan Dazert ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Implant ◽  
Cochlear Implantation ◽  
Verbal Fluency ◽  
Homogeneous Population ◽  
Delayed Recall ◽  
Hearing Status ◽  
Age Related ◽  
Significant Difference ◽  
The Impact

<b><i>Introduction:</i></b> Age-related hearing loss affects about one-third of the population worldwide. Studies suggest that hearing loss may be linked to cognitive decline and auditory rehabilitation may improve cognitive functions. So far, the data are limited, and the underlying mechanisms are not fully understood. The study aimed to analyze the impact of cochlear implantation on cognition in a large homogeneous population of hearing-impaired adults using a comprehensive non-auditory cognitive assessment with regard to normal-hearing (NH) subjects. <b><i>Material and Methods:</i></b> Seventy-one cochlear implant (CI) candidates with a postlingual, bilateral severe or profound hearing loss aged 66.3 years (standard deviation [SD] 9.2) and 105 NH subjects aged 65.96 years (SD 9.4) were enrolled. The computer-based neurocognitive tool applied included 11 subtests covering attention (M3), short- and long-term memory (recall and delayed recall), working memory (0- and 2-back, Operation Span [OSPAN] task), processing speed (Trail Making Test [TMT] A), mental flexibility (TMT B), inhibition (cFlanker and iFlanker), and verbal fluency. CI patients underwent a neurocognitive testing preoperatively as well as 12 months postoperatively. Impact of hearing status, age, gender, and education on cognitive subdomains was studied. Additionally, after controlling for education and age, cognitive performance of CI subjects (<i>n</i> = 41) was compared to that of NH (<i>n</i> = 34). <b><i>Results:</i></b> CI users achieved significantly better neurocognitive scores 12 months after cochlear implantation than before in most subtests (M3, [delayed] recall, 2-back, OSPAN, iFlanker, and verbal fluency; all <i>p</i> &#x3c; 0.05) except for the TMT A and B. A significant correlation could be found between the postoperative improvement in speech perception and in the attentional task M3 (<i>p</i> = 0.01). Hearing status (<i>p</i> = 0.0006) had the strongest effect on attention, whereas education had a high impact on recall (<i>p</i> = 0.002), OSPAN (<i>p</i> = 0.0004), and TMT A (<i>p</i> = 0.005) and B (<i>p</i> = 0.003). Inhibition was mainly age-dependent with better results in younger subjects (<i>p</i> = 0.016). Verbal fluency was predicted by gender as females outperformed men (<i>p</i> = 0.009). Even after controlling for age and education NH subjects showed a significantly better performance than CI candidates in the recall (<i>p</i> = 0.03) and delayed recall (<i>p</i> = 0.01) tasks. Postoperatively, there was no significant difference between the 2 groups anymore. <b><i>Conclusion:</i></b> Impact of cochlear implantation on neurocognitive functions differs according to the cognitive subdomains. Postoperatively, CI recipients performed as good as age- and education-matched NH subjects.

Outer hair cells in the mammalian cochlea and noise-induced hearing loss

Nature ◽  
1985 ◽  
Vol 315 (6021) ◽  
pp. 662-665 ◽  
Author(s):  
A. R. Cody ◽  
I. J. Russell
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Outer Hair Cells ◽  
Noise Induced Hearing Loss

Hearing loss patterns after cochlear implantation via the round window in an animal model

2016 ◽  
Vol 37 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Joseph Attias ◽  
Roy Hod ◽  
Eyal Raveh ◽  
Aviram Mizrachi ◽  
Karen B. Avraham ◽  
...  
Keyword(s):  
Animal Model ◽  
Hearing Loss ◽  
Cochlear Implantation ◽  
Round Window

scholarly journals Disruption of Hars2 in Cochlear Hair Cells Causes Progressive Mitochondrial Dysfunction and Hearing Loss in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Pengcheng Xu ◽  
Longhao Wang ◽  
Hu Peng ◽  
Huihui Liu ◽  
Hongchao Liu ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Mitochondrial Dysfunction ◽  
Hair Cells ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Hair Cell Loss ◽  
Progressive Hearing Loss ◽  
Cochlear Hair Cells ◽  
Inner Hair Cells

Mutations in a number of genes encoding mitochondrial aminoacyl-tRNA synthetases lead to non-syndromic and/or syndromic sensorineural hearing loss in humans, while their cellular and physiological pathology in cochlea has rarely been investigated in vivo. In this study, we showed that histidyl-tRNA synthetase HARS2, whose deficiency is associated with Perrault syndrome 2 (PRLTS2), is robustly expressed in postnatal mouse cochlea including the outer and inner hair cells. Targeted knockout of Hars2 in mouse hair cells resulted in delayed onset (P30), rapidly progressive hearing loss similar to the PRLTS2 hearing phenotype. Significant hair cell loss was observed starting from P45 following elevated reactive oxygen species (ROS) level and activated mitochondrial apoptotic pathway. Despite of normal ribbon synapse formation, whole-cell patch clamp of the inner hair cells revealed reduced calcium influx and compromised sustained synaptic exocytosis prior to the hair cell loss at P30, consistent with the decreased supra-threshold wave I amplitudes of the auditory brainstem response. Starting from P14, increasing proportion of morphologically abnormal mitochondria was observed by transmission electron microscope, exhibiting swelling, deformation, loss of cristae and emergence of large intrinsic vacuoles that are associated with mitochondrial dysfunction. Though the mitochondrial abnormalities are more prominent in inner hair cells, it is the outer hair cells suffering more severe cell loss. Taken together, our results suggest that conditional knockout of Hars2 in mouse cochlear hair cells leads to accumulating mitochondrial dysfunction and ROS stress, triggers progressive hearing loss highlighted by hair cell synaptopathy and apoptosis, and is differentially perceived by inner and outer hair cells.

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