Regeneration of the inner ear as a model of neural plasticity

Authors

  • D. Kent Morest,

    Corresponding author
    1. Department of Neuroscience, The University of Connecticut Health Center, Farmington, Connecticut
    2. Department of Communication Sciences, The University of Connecticut, Storrs, Connecticut
    • Department of Neuroscience, The University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3401
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  • Douglas A. Cotanche

    1. Department of Otolaryngology, Children's Hospital, Boston, Massachusetts
    2. Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts
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Abstract

The publication of a paper entitled “Direct transdifferentiation gives rise to the earliest new hair cells in regenerating avian auditory epithelium” in the Journal of Neuroscience Research offers the opportunity to call attention to a well-developed line of research on the auditory receptor of birds, which should be of interest to students of regeneration and plasticity of the mature nervous system in higher vertebrates, including mammals. Although hair cell proliferation normally stops before hatching, destruction of the auditory receptors of the chicken may be followed by complete regeneration of hair cells. Most of the new hair cells arise from a new wave of proliferation, but Roberson et al. show that about one-third of the new hair cells are formed without undergoing cell division and thus may differentiate from so-called supporting cells or cells with an “intermediate morphology.” This finding suggests some models for regeneration of this neuroepithelium, including the possibility that mature supporting cells could transform directly into hair cells. The present Mini-Review discusses some of the models for neural regeneration that future studies might address in the light of our current knowledge and the new report. The possibility is raised that transitional forms of hair cell and supporting cell precursors may reside in the inner ear in a quiescent state until stimulated by damage. © 2004 Wiley-Liss, Inc.

Ancillary