ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Aminoglycoside-induced phosphatidylserine externalization in sensory hair cells is regionally restricted, rapid, and reversible.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- TMC1 and TMC2 are cholesterol-dependent scramblases that regulate membrane homeostasis in auditory hair cells.bioRxiv : the preprint server for biology · 2025Article
- Mammalian TMC1 or 2 are necessary for scramblase activity in auditory hair cells.Hearing research · 2025Article
- Hair cell apoptosis and deafness inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Aminoglycoside induces RIPOR2 translocation and phosphatidylserine externalization via distinct mechanisms.Frontiers in cellular neuroscience · 2025Article
- Mitochondrial form and function in hair cells.Hearing research · 2023Review
- Regulation of membrane homeostasis by TMC1 mechanoelectrical transduction channels is essential for hearing.Science advances · 2022Article
- Identifying targets to prevent aminoglycoside ototoxicity.Molecular and cellular neurosciences · 2022Review
- Neonatal AAV gene therapy rescues hearing in a mouse model of SYNE4 deafness.EMBO molecular medicine · 2021Article
- Structural and functional consequences of reversible lipid asymmetry in living membranes.Nature chemical biology · 2020Review
- Macrophages Respond Rapidly to Ototoxic Injury of Lateral Line Hair Cells but Are Not Required for Hair Cell Regeneration.Frontiers in cellular neuroscience · 2020Article
- Molecular Structure of the Hair Cell Mechanoelectrical Transduction Complex.Cold Spring Harbor perspectives in medicine · 2019Review
- Phosphoinositol-4,5-Bisphosphate Regulates Auditory Hair-Cell Mechanotransduction-Channel Pore Properties and Fast Adaptation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Towards the Prevention of Aminoglycoside-Related Hearing Loss.Frontiers in cellular neuroscience · 2017Review
- Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.Disease models & mechanisms · 2015Article
- Ganglioside GM3 is essential for the structural integrity and function of cochlear hair cells.Human molecular genetics · 2015Article
- Staurosporine-induced collapse of cochlear hair bundles.The Journal of comparative neurology · 2014Article
- ER-mitochondrial calcium flow underlies vulnerability of mechanosensory hair cells to damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Lead roles for supporting actors: critical functions of inner ear supporting cells.Hearing research · 2013Review
- Disruption of intracellular calcium regulation is integral to aminoglycoside-induced hair cell death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Bumetanide hyperpolarizes madin-darby canine kidney cells and enhances cellular gentamicin uptake by elevating cytosolic Ca(2+) thus facilitating intermediate conductance Ca(2+)--activated potassium channels.Cell biochemistry and biophysics · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The aminophospholipid phosphatidylserine (PS) is normally restricted to the inner leaflet of the plasma membrane. During certain cellular processes, including apoptosis, PS translocates to the outer leaflet and can be labeled with externally applied annexin V, a calcium-dependent PS-binding protein. In mouse cochlear cultures, annexin V labeling reveals that the aminoglycoside antibiotic neomycin induces rapid PS externalization, specifically on the apical surface of hair cells. PS externalization is observed within approximately 75 s of neomycin perfusion, first on the hair bundle and then on membrane blebs forming around the apical surface. Whole-cell capacitance also increases significantly within minutes of neomycin application, indicating that blebbing is accompanied by membrane addition to the hair cell surface. PS externalization and membrane blebbing can, nonetheless, occur independently. Pretreating hair cells with calcium chelators, a procedure that blocks mechanotransduction, or overexpressing a phosphatidylinositol 4,5-biphosphate (PIP2)-binding pleckstrin homology domain, can reduce neomycin-induced PS externalization, suggesting that neomycin enters hair cells via transduction channels, clusters PIP2, and thereby activates lipid scrambling. The effects of short-term neomycin treatment are reversible. After neomycin washout, PS is no longer detected on the apical surface, apical membrane blebs disappear, and surface-bound annexin V is internalized, distributing throughout the supranuclear cytoplasm of the hair cell. Hair cells can therefore repair, and recover from, neomycin-induced surface damage. Hair cells lacking myosin VI, a minus-end directed actin-based motor implicated in endocytosis, can also recover from brief neomycin treatment. Internalized annexin V, however, remains below the apical surface, thereby pinpointing a critical role for myosin VI in the transport of endocytosed material away from the periphery of the hair cell.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.