Glutamate induces apoptosis in cultured spiral ganglion explants

Biochem Biophys Res Commun. 2007 May 25;357(1):14-9. doi: 10.1016/j.bbrc.2007.03.098. Epub 2007 Mar 26.


Traumatic sound exposure, aminoglycoside antibiotics, cochlea ischemia or traumatic stress leads to an excessive release of glutamate from inner hair cells into the synaptic cleft. The high glutamate concentration can cause a swelling and destruction of the dendrites of spiral ganglion neurons of type I as well as a reduction in the number of neurons. This may be a cause of hearing loss. The mechanism causing the reduction of neurons is still not known. Apoptosis, also called programmed cell death, could be involved. In this study, cultured spiral ganglion explants were incubated with glutamate in high concentrations. Neurite outgrowth was determined and additionally a new method was established for studying the morphology of single spiral ganglion neurons. For the first time it was shown that glutamate induces apoptosis of spiral ganglion neurons, which could be blocked selectively by a caspase-3 inhibitor. This could offer a new therapeutic strategy for hearing disorders.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Gerbillinae
  • Glutamic Acid / administration & dosage*
  • Neurites / drug effects
  • Neurites / ultrastructure
  • Spiral Ganglion / cytology*
  • Spiral Ganglion / drug effects*
  • Tissue Culture Techniques


  • Glutamic Acid