scholarly journals Age‐related changes in the biophysical and morphological characteristics of mouse cochlear outer hair cells

2020 ◽  
Vol 598 (18) ◽  
pp. 3891-3910 ◽  
Author(s):  
Jing‐Yi Jeng ◽  
Stuart L. Johnson ◽  
Adam J Carlton ◽  
Lara De Tomasi ◽  
Richard J. Goodyear ◽  
...  
1994 ◽  
Vol 111 (6) ◽  
pp. 799-806 ◽  
Author(s):  
Meiho Nakayama ◽  
Robert H. Helfert ◽  
Horst R. Konrad ◽  
Donald M. Caspary

An ultrastructural study was performed to assets age-related changes in the vestibular end organs of Fischer 344 rats. The surfaces of the maculae and cristae from 3-, 12-, and 24-month-old Fischer 344 rats were observed by use of scanning electron microscopy. Age-related changes in the morphology of the vestibular neuroepithelium included a substantial loss of hair cells, as well as a reduction in the number of kinocllia and stereocilla on those that remained. These changes were greatest in the central upper regions of the three ampullae. In aged animals a greater area of the neuroepithelial surface was covered with microvilli, and in some instances, giant cilia were found among the microvillous surfaces. In contrast, there were few differences among the three age groups in the number and condition of hair cells in the saccules and utricles. The changes observed in the cristae may contribute to the age-associated impairment of vestibular function. If similar changes occur in human beings, these could in part account for the presbycusis observed in the elderly.


2018 ◽  
Vol 370 ◽  
pp. 11-15 ◽  
Author(s):  
R.A. Altschuler ◽  
A. Kanicki ◽  
C. Martin ◽  
D.C. Kohrman ◽  
R.A. Miller

2020 ◽  
Vol 117 (21) ◽  
pp. 11811-11819 ◽  
Author(s):  
Luis E. Boero ◽  
Valeria C. Castagna ◽  
Gonzalo Terreros ◽  
Marcelo J. Moglie ◽  
Sebastián Silva ◽  
...  

“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.


2017 ◽  
Vol 31 (2) ◽  
pp. 86-90 ◽  
Author(s):  
Qamar Ul Islam ◽  
Muhammad Kamran Saeed ◽  
Mohammad Asim Mehboob

2020 ◽  
Vol 5 (5) ◽  
pp. 1166-1174
Author(s):  
Sherri M. Jones

Purpose Aging is ubiquitous and the elderly population (aged 65 years and older) will continue to grow, reaching an estimated 25% of the U.S. population by 2060. Symptoms of dizziness and imbalance as well as risk of falling are more common in older adults, but it is often unclear whether these symptoms are due to disease or a consequence of aging. Indeed, age-related changes in the vestibular periphery are not well understood. This invited review describes age-related changes in peripheral vestibular function, comparisons between aging of auditory and vestibular function, structural correlates for vestibular aging, and the role of genetics in vestibular aging. Conclusion The data from animal models will show that gravity receptor function declines with age but at different rates for different inbred mouse strains. Gravity receptor aging includes loss of postsynaptic elements and loss of hair cells, which is observed at advanced ages. Loss of hair cells may contribute to some extent at advanced ages. Age-related changes in hearing do not predict age-related changes in vestibular function. Genes likely influence the rate of decline in vestibular function. Further research is needed to fully understand the fundamental mechanisms of vestibular aging and to begin to develop potential therapeutic approaches.


2020 ◽  
Vol 21 (7) ◽  
pp. 2505
Author(s):  
Ah-Ra Lyu ◽  
Tae Hwan Kim ◽  
Sung Jae Park ◽  
Sun-Ae Shin ◽  
Seong-Hun Jeong ◽  
...  

Age-related hearing loss (ARHL) is an irreversible, progressive neurodegenerative disorder and is presently untreatable. Previous studies using animal models have suggested mitochondrial damage and programmed cell death to be involved with ARHL. Thus, we further investigated the pathophysiologic role of mitochondria and necroptosis in aged C57BL/6J male mice. Aged mice (20 months old) exhibited a significant loss of hearing, number of hair cells, neuronal fibers, and synaptic ribbons compared to young mice. Ultrastructural analysis of aged cochleae revealed damaged mitochondria with absent or disorganized cristae. Aged mice also showed significant decrease in cochlear blood flow, and exhibited increase in gene expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) and the pseudokinase mixed-lineage kinase domain-like (MLKL). Immunofluorescence (IF) assays of cytochrome C oxidase I (COX1) confirmed mitochondrial dysfunction in aged cochleae, which correlated with the degree of mitochondrial morphological damage. IF assays also revealed localization and increased expression of RIPK3 in sensorineural tissues that underwent significant necroptosis (inner and outer hair cells and stria vascularis). Together, our data shows that the aging cochlea exhibits damaged mitochondria, enhanced synthesis of proinflammatory cytokines, and provides new evidence of necroptosis in the aging cochlea in in vivo.


2021 ◽  
Vol 5 (2) ◽  
pp. e202101068
Author(s):  
Kuu Ikäheimo ◽  
Anni Herranen ◽  
Vilma Iivanainen ◽  
Tuuli Lankinen ◽  
Antti A Aarnisalo ◽  
...  

Failure in the structural maintenance of the hair cell stereocilia bundle and ribbon synapse causes hearing loss. Here, we have studied how ER stress elicits hair cell pathology, using mouse models with inactivation of Manf (mesencephalic astrocyte-derived neurotrophic factor), encoding an ER-homeostasis-promoting protein. From hearing onset, Manf deficiency caused disarray of the outer hair cell stereocilia bundle and reduced cochlear sound amplification capability throughout the tonotopic axis. In high-frequency outer hair cells, the pathology ended in molecular changes in the stereocilia taper region and in strong stereocilia fusion. In high-frequency inner hair cells, Manf deficiency degraded ribbon synapses. The altered phenotype strongly depended on the mouse genetic background. Altogether, the failure in the ER homeostasis maintenance induced early-onset stereociliopathy and synaptopathy and accelerated the effect of genetic causes driving age-related hearing loss. Correspondingly, MANF mutation in a human patient induced severe sensorineural hearing loss from a young age onward. Thus, we present MANF as a novel protein and ER stress as a mechanism that regulate auditory hair cell maintenance in both mice and humans.


2011 ◽  
Vol 60 (4) ◽  
pp. 355-361 ◽  
Author(s):  
Hitoshi OKUMURA ◽  
Yuki MIYASAKA ◽  
Yuka MORITA ◽  
Tomoyuki NOMURA ◽  
Yukio MISHIMA ◽  
...  

2019 ◽  
Vol 53 (4) ◽  
pp. 287-296
Author(s):  
Haruko Yasumori ◽  
Eiko Tamura ◽  
Kazue Tsukahara ◽  
Yayoi Inoue ◽  
Takamasa Yamamoto

1982 ◽  
Vol 90 (6) ◽  
pp. 787-794 ◽  
Author(s):  
Paul R. Lambert ◽  
Ilsa R. Schwartz

The cochleas and brain stems of normal-hearing CBA/CaJ and CaH mice ranging in age from 1 to 18 months were examined by light microscopy to document normal age-related changes. At all ages examined, the cochlear morphologic structure appeared normal with no obvious loss of hair cells or spiral ganglion cells. In the cochlear nucleus, qualitative and quantitative changes were observed in the total nuclear volume, in globular cell size, and in neuronal packing density.


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