New perspectives on cochlear nerve degeneration in acquired sensorineural hearing loss

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• Charles Liberman. Harvard Medical School
• Monday 09 March 2015, 16:30-18:00
• The Hodgkin Huxley Seminar Room, Department of Physiology Development and Neuroscience.

If you have a question about this talk, please contact P.H. Marchington.

Wan, G., Gomez-Casati, M.E., Gigliello, A. R., Liberman M.C. & Corfas, G. 2014. Neurotrophin- 3 regulates ribbon synapse density in the cochlea and induces synapse regeneration after acoustic trauma. 10.7554/eLife. 03564 Abstract Neurotrophin-3 (Ntf3) and brain derived neurotrophic factor (Bdnf) are critical for sensory neuron survival and establishment of neuronal projections to sensory epithelia in the embryonic inner ear, but their postnatal functions remain poorly understood. Using cell-specific inducible gene recombination in mice we found that, in the postnatal inner ear, Bbnf and Ntf3 are required for the formation and maintenance of hair cell ribbon synapses in the vestibular and cochlear epithelia, respectively. We also show that supporting cells in these epithelia are the key endogenous source of the neurotrophins. Using a new hair cell CreERT line with mosaic expression, we also found that Ntf3’s effect on cochlear synaptogenesis is highly localized. Moreover, supporting cell-derived Ntf3, but not Bbnf, promoted recovery of cochlear function and ribbon synapse regeneration after acoustic trauma. These results indicate that glial-derived neurotrophins play critical roles in inner ear synapse density and synaptic regeneration after injury. DOI : 10.7554/eLife.03564.001

Kujawa,S.G. & Liberman, M.C. 2009. Adding insult to injury: cochlear nerve degeneration after ‘temporary’ noise-induced hearing loss. The Journal of Neuroscience, Nov 11, 2009- 29(45): 14077-14085. Overexposure to intense sound can cause temporary or permanent hearing loss. Postexposure recovery of threshold sensitivity has been assumed to indicate reversal of damage to delicate mechano-sensory and neural structures of the inner ear and no persistent or delayed consequences for auditory function. Here, we show, using cochlear functional assays and confocal imaging of the inner ear in mouse, that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the cochlear nerve. Results suggest that noise-induced damage to the ear has progressive consequences that are considerably more widespread than are revealed by conventional threshold testing. This primary neurodegeneration should add to difficulties hearing in noisy environments, and could contribute to tinnitus, hyperacusis, and other perceptual anomalies commonly associated with inner ear damage.

This talk is part of the Adrian Seminars in Neuroscience series.

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