Department of Biological Structure, University of Washington, Seattle, United States; Graduate Program in Neuroscience, University of Washington, Seattle, United States
Eric D Thomas
Department of Biological Structure, University of Washington, Seattle, United States; Graduate Program in Neuroscience, University of Washington, Seattle, United States
Joy Y Sebe
Department of Biological Structure, University of Washington, Seattle, United States
Tor Linbo
Department of Biological Structure, University of Washington, Seattle, United States
Robert Esterberg
Department of Biological Structure, University of Washington, Seattle, United States; Virginia Merrill Bloedel Hearing Research Center, University of Washington, Seattle, United States
Dale W Hailey
Department of Biological Structure, University of Washington, Seattle, United States; Virginia Merrill Bloedel Hearing Research Center, University of Washington, Seattle, United States
Department of Biological Structure, University of Washington, Seattle, United States; Graduate Program in Neuroscience, University of Washington, Seattle, United States; Virginia Merrill Bloedel Hearing Research Center, University of Washington, Seattle, United States
Mitochondria play a prominent role in mechanosensory hair cell damage and death. Although hair cells are thought to be energetically demanding cells, how mitochondria respond to these demands and how this might relate to cell death is largely unexplored. Using genetically encoded indicators, we found that mitochondrial calcium flux and oxidation are regulated by mechanotransduction and demonstrate that hair cell activity has both acute and long-term consequences on mitochondrial function. We tested whether variation in mitochondrial activity reflected differences in the vulnerability of hair cells to the toxic drug neomycin. We observed that susceptibility did not correspond to the acute level of mitochondrial activity but rather to the cumulative history of that activity.