A mechanism for sensing noise damage in the inner ear

Curr Biol. 2004 Mar 23;14(6):526-9. doi: 10.1016/j.cub.2004.03.002.


Our sense of hearing requires functional sensory hair cells. Throughout life those hair cells are subjected to various traumas, the most common being loud sound. The primary effect of acoustic trauma is manifested as damage to the delicate mechanosensory apparatus of the hair cell stereocilia. This may eventually lead to hair cell death and irreversible deafness. Little is known about the way in which noxious sound stimuli affect individual cellular components of the auditory sensory epithelium. However, studies in different types of cell cultures have shown that damage and mechanical stimulation can activate changes in intracellular free calcium concentration ([Ca(2+)](i)) and elicit intercellular Ca(2+) waves. Thus an attractive hypothesis is that changes in [Ca(2+)](i), propagating as a wave through support cells in the organ of Corti, may constitute a fundamental mechanism to signal the occurrence of hair cell damage. The mechanism we describe here exhibits nanomolar sensitivity to extracellular ATP, involves regenerative propagation of intercellular calcium waves due to ATP originating from hair cells, and depends on functional IP(3)-sensitive intracellular stores in support cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Calcium Signaling / physiology*
  • Fluorescent Antibody Technique
  • Hair Cells, Auditory / injuries*
  • Humans
  • Inositol 1,4,5-Trisphosphate / metabolism*
  • Organ of Corti / metabolism
  • Organ of Corti / physiology*
  • Receptors, Purinergic P2 / genetics
  • Receptors, Purinergic P2 / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sound


  • Receptors, Purinergic P2
  • Inositol 1,4,5-Trisphosphate
  • Adenosine Triphosphate