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SUMMARY:New perspectives on cochlear nerve degeneration in acquired sensor
 ineural hearing loss - Charles Liberman. Harvard Medical School
DTSTART:20150309T163000Z
DTEND:20150309T180000Z
UID:TALK57350@talks.cam.ac.uk
CONTACT:P.H. Marchington
DESCRIPTION: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\nAbstract Neurotrophin-3 (Ntf3) and brain derived neurot
 rophic factor (Bdnf) are critical for sensory neuron survival and establis
 hment of neuronal projections to sensory epithelia in the embryonic inner 
 ear\, but their postnatal functions remain poorly understood. Using cell-s
 pecific inducible gene recombination in mice we found that\, in the postna
 tal inner ear\, Bbnf and Ntf3 are required for the formation and maintenan
 ce of hair cell ribbon synapses in the vestibular and cochlear epithelia\,
  respectively. We also show that supporting cells in these epithelia are t
 he key endogenous source of the neurotrophins. Using a new hair cell CreER
 T line with mosaic expression\, we also found that Ntf3's effect on cochle
 ar synaptogenesis is highly localized. Moreover\, supporting cell-derived 
 Ntf3\, but not Bbnf\, promoted recovery of cochlear function and ribbon sy
 napse regeneration after acoustic trauma. These results indicate that glia
 l-derived neurotrophins play critical roles in inner ear synapse density a
 nd synaptic regeneration after injury. DOI: 10.7554/eLife.03564.001 \n\nKu
 jawa\,S.G. & Liberman\, M.C. 2009. Adding insult to injury: cochlear nerve
  degeneration after ‘temporary’ noise-induced hearing loss. The Journa
 l of Neuroscience\, Nov 11\, 2009- 29(45): 14077-14085.\nOverexposure to i
 ntense sound can cause temporary or permanent hearing loss. Postexposure r
 ecovery 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 complet
 ely 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 e
 ar has progressive consequences that are considerably more widespread than
  are revealed by conventional threshold testing. This primary neurodegener
 ation should add to difficulties hearing in noisy environments\, and could
  contribute to tinnitus\, hyperacusis\, and\nother perceptual anomalies co
 mmonly associated with inner ear damage.\n
LOCATION:The Hodgkin Huxley Seminar Room\, Department of Physiology Develo
 pment and Neuroscience
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