ArticlePloS one2016
Sound-Induced Intracellular Ca2+ Dynamics in the Adult Hearing Cochlea.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanisms driving the functional maturation of the developing mammalian auditory pathway.Current topics in developmental biology · 2025Review
- Noise induces Ca2+ signaling waves and Chop/S-Xbp1 expression in the hearing cochlea.JCI insight · 2024Article
- Synaptic ribbon dynamics after noise exposure in the hearing cochlea.Communications biology · 2024Article
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- TMTC4 is a hair cell-specific human deafness gene.JCI insight · 2023Article
- Age-related changes in P2Y receptor signalling in mouse cochlear supporting cells.The Journal of physiology · 2023Article
- A NovelFrontiers in molecular neuroscience · 2021Article
- Integrated stress response inhibition provides sex-dependent protection against noise-induced cochlear synaptopathy.Scientific reports · 2020Article
- Purinergic Signaling and Cochlear Injury-Targeting the Immune System?International journal of molecular sciences · 2019Review
- Targeting Inflammatory Processes Mediated by TRPVI and TNF-α for Treating Noise-Induced Hearing Loss.Frontiers in cellular neuroscience · 2019Article
- Intercellular CaThe Journal of physiology · 2019Article
- Deletion of Tmtc4 activates the unfolded protein response and causes postnatal hearing loss.The Journal of clinical investigation · 2018Article
- Osmotic stabilization prevents cochlear synaptopathy after blast trauma.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ signaling has been implicated in the initial pathophysiologic mechanisms underlying the cochlea's response to acoustic overstimulation. Intracellular Ca2+ signaling (ICS) waves, which occur in glia and retinal cells in response to injury to activate cell regulatory pathways, have been proposed as an early event in cochlear injury. Disruption of ICS activity is thought to underlie Connexin 26-associated hearing loss, the most common genetic form of deafness, and downstream sequelae of ICS wave activity, such as MAP kinase pathway activation, have been implicated in noise-induced hearing loss. However, ICS waves have only been observed in neonatal cochlear cultures and are thought to be quiescent after the onset of hearing. In this study, we employ an acute explant model of an adult, hearing cochlea that retains many in vivo physiologic features to investigate Ca2+ changes in response to sound. We find that both slow monotonic changes in intracellular Ca2+ concentration as well as discrete ICS waves occur with acoustic overstimulation. The ICS waves share many intrinsic features with their better-described neonatal counterparts, including ATP and gap-junction dependence, and propagation velocity and distance. This identification of ICS wave activity in the adult, hearing cochlea thus confirms and characterizes an important early detection mechanism for cochlear trauma and provides a target for interventions for noise-induced and Connexin 26-associated hearing loss.
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Registered trials
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