Differential vulnerability of inner and outer hair cell systems to chronic mild hypoxia and glutamate ototoxicity: insights into the cause of auditory neuropathy

J Otolaryngol. 2001 Apr;30(2):106-14. doi: 10.2310/7070.2001.20818.

Abstract

Objective: To describe the effects of long-term mild hypoxia and of glutamate poisoning on the functional properties of the cochlea.

Methods: Outer hair cell activity was monitored using otoacoustic emissions and cochlear microphonics, and inner hair cell/cochlear afferent function was measured using neural responses (cochlear action potentials or auditory brainstem responses [ABRs]).

Results: In contrast to the effects of acute anoxia, in which all aspects of cochlear function are simultaneously lost, mild, long-term hypoxia results in a clear differential effect on outer versus inner hair cell systems. During a 2-hour period of mild hypoxia, ABR amplitude and threshold deteriorate significantly, whereas outer hair cell function, as reflected by otoacoustic emissions, shows little or no change. A similar dissociation between inner and outer hair cell function is observed during instillation of glutamate (1-10 mM), where the cochlear microphonic and the otoacoustic emissions are unchanged, whereas cochlear action potential amplitudes are reduced.

Conclusion: These studies demonstrate a difference in vulnerability of inner and outer hair cell systems. The inner hair cell/cochlear afferent system is vulnerable to long-term, mild hypoxia; this may be an etiologic factor in hearing loss of cochlear origin, particularly in high-risk birth infants with auditory neuropathy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Hypoxia
  • Chinchilla
  • Cochlear Microphonic Potentials
  • Glutamic Acid / toxicity*
  • Hair Cells, Auditory, Inner / drug effects*
  • Hair Cells, Auditory, Inner / physiopathology
  • Hair Cells, Auditory, Outer / drug effects*
  • Hair Cells, Auditory, Outer / physiopathology
  • Microscopy, Electron, Scanning
  • Otoacoustic Emissions, Spontaneous
  • Time Factors
  • Vestibulocochlear Nerve Diseases / etiology*

Substances

  • Glutamic Acid