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Tinnitus
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Tinnitus most often results from damage to the hair cells located in a structure of your inner ear called the cochlea that are together responsible for the sensation of sound. A common way that this hair cell damage happens is that a person has too much exposure to loud noise, such as explosions or heavy machinery. Tinnitus can also be associated with head injuries, neck injuries, certain medications, and oftentimes tinnitus just kind of shows up and the person doesn't know why—this last mysterious category is known as idiopathic tinnitus (Henry et al., 2005). Tinnitus may also occur when a person hasn't experienced hearing loss, but that is significantly more rare and may even involve different problematic areas in the brain when compared to the more common type associated with hearing loss (Vanneste & De Ridder, 2016).
Sensorineural Hearing Loss
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Linnea Cheung, David M. Baguley, Andrew McCombe
Table 14.2 summarises known ototoxic agents and their mechanisms of action. These agents enter the inner ear through various mechanisms where they can cause damage. Entry is predominantly via the blood supply into the perilymph, although the precise mechanism of diffusion across this blood-perilymph barrier is unknown. Endolymph can be accessed via perilymph through selectively permeable membranes and tight junctions between adjacent cells. Diffusion can also occur via the round and oval windows from the middle ear. Any hearing deficit caused by hair cell loss is usually permanent as the organ of Corti cannot spontaneously regenerate hair cells
Assessing Paediatric Development in Psychiatry
Published in Cathy Laver-Bradbury, Margaret J.J. Thompson, Christopher Gale, Christine M. Hooper, Child and Adolescent Mental Health, 2021
The fibres carrying information on the tone, pitch and frequency of incoming sound waves, detected by the ear, once coded, make up the cochlear nerve. Hair cells, i.e. the histological sensory unit, are located within the central core of the cochlear apparatus, a coiled structure located in the inner ear. The direction and degree of distortion of fluid surrounding the hair cells are dependent on the frequency and the intensity of the incoming sound wave, which causes the hair cells to fluctuate. This produces a responsive action potential.
The applications of targeted delivery for gene therapies in hearing loss
Published in Journal of Drug Targeting, 2023
Melissa Jones, Bozica Kovacevic, Corina Mihaela Ionescu, Susbin Raj Wagle, Christina Quintas, Elaine Y. M. Wong, Momir Mikov, Armin Mooranian, Hani Al-Salami
The sensory hair cells transduce auditory signals, with mechanosensitive stereocilia bundles positioned on their apical surface. The bundles themselves are arranged in a highly uniform chevron shape, with each bundle containing 50 to 200 stereocilia [39]. Outer hair cells contribute to the process of cochlea amplification, assisting in the selectivity and diversity of hearing via the mechanical boosting of sound-induced vibrations [44]. This offers a wide dynamic range, sharp frequency tuning and overall high sensitivity. Inner hair cells possess mechanotransduction channels, indicating their ability to result in a biological response from a physical stimulus. Which, in the case of inner hair cells, occurs via the auditory nerve fibre synaptic connection, permitting the detection of sound, and transmitting information about the acoustic environment to the central auditory system. Overall, sound vibrations are detected by inner hair cells following amplification by outer hair cells [45–47]. One key element of significance to note is the inability for the regeneration of mammalian ear hair cells. This is in contrast to non-mammalian vertebrate species which have the capacity for hair cell restoration via the regeneration of supporting cells. Hence, damage to mammalian hair cells is currently considered permanent and leads to varying degrees of hearing loss [48–50].
The PERK/ATF4/CHOP signaling branch of the unfolded protein response mediates cisplatin-induced ototoxicity in hair cells
Published in Drug and Chemical Toxicology, 2023
Yanji Qu, Shimin Zong, Zhe Wang, Peiyu Du, Yingying Wen, Hao Li, Nan Wu, Hongjun Xiao
Cochlear hair cells in the inner ear serve an important role in transducing sound waves into electric signals (Wang et al.2017, Liu et al.2019b). Impaired function of hair cells can be caused by numerous factors, including mutations in deafness genes, aging, noise exposure, chronic cochlear infections and ototoxic drugs (Ding et al. 2020). Cisplatin and aminoglycosides are considered to be the most important ototoxic drugs (He et al.2017, Li et al.2018a, 2018b). However, to date, there is still no effective treatment strategy for cisplatin-induced hearing loss based on known mechanisms underlying cisplatin-induced ototoxicity. A previous study from our laboratory demonstrated that the UPR was involved in cisplatin-induced cochlear cell apoptosis in vivo (Zong et al.2017). However, how UPR mediates cisplatin-induced ototoxicity requires further investigation. The current study aimed to explore the sequential changes in the key UPR signaling branch and its potential pro-apoptotic role in cisplatin-induced ototoxicity. Notably, the ATF4/CHOP signaling branch was activated in cisplatin-treated OC-1 cells in a time-dependent manner. The results indicated that the UPR may serve an important role in affecting cell fate under cisplatin treatment. Furthermore, CHOP was demonstrated to act as a key molecule in cisplatin-induced hair cell apoptosis.
Glycogen synthase kinase 3 (GSK-3) inhibitors: a patent update (2016–2019)
Published in Expert Opinion on Therapeutic Patents, 2020
Carlos Roca, Nuria E. Campillo
Another application is this field is the hearing loss. Hair cells are receptor cells that transduce the acoustic stimulus. Permanent damage to the inner ear hair cells results in sensorineural hearing loss. Neurosensory hearing loss affects a broad range of people worldwide and results mainly from an irreversible loss of cochlear hair cells. Different molecular pathways are involved in hair cell regeneration. The Lgr5-positive cells represent the most potent pool of progenitor cells. Different stimuli such as hair call loss, inhibition of Notch pathway, forced expression of Atoh1, activation of Wnt canonical pathway, or inhibition of EphrinB2 signaling can trigger supporting cells proliferation and/or their trans-differentiation [42]. Roccio et al. reported the cell cycle reactivation of cochlear progenitor cells in neonatal FUCCI mice by a GSK-3 small molecule inhibitor [43]. Based on these results, Frequency Therapeutics Inc. claims a method that comprises the use of compounds to activate the Wnt pathway or the inhibition of GSK3-β activity. The method further comprises a differentiation inhibitor (e.g. an HDAC inhibitor (e.g. valproic acid) or a Notch agonist thereby facilitating generation of inner ear hair cells from the expanded population of stem cells [44–47]. The inventors have advantage of the synergy of the different compounds that act at different level of the proliferation pathway.