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Aminoglycoside neurotoxicity involves NMDA receptor activation

J A Segal1, B D Harris, Y Kustova

  • 1Laboratory of Neuroscience, National Institute on Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. segalj@lilly.com

Brain Research
|January 8, 1999
PubMed
Summary

Aminoglycoside antibiotics, like neomycin, can cause brain damage by activating NMDA receptors. This excitotoxic process contributes to ototoxicity and may affect the central nervous system with a compromised blood-brain barrier.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Toxicology

Background:

  • Aminoglycoside antibiotics are hypothesized to cause ototoxicity via excitotoxic activation of cochlear NMDA receptors.
  • This suggests aminoglycosides might also injure brain neurons, but their poor blood-brain barrier penetration limits direct study.

Purpose of the Study:

  • To investigate the potential neurotoxic effects of aminoglycosides within the brain.
  • To determine if neomycin directly damages striatal neurons and if NMDA receptor activation mediates this damage.

Main Methods:

  • Intrastriatal injection of neomycin in rats to bypass the blood-brain barrier.
  • Assessment of striatal damage using glial fibrillary acidic protein (GFAP) and OX-6 staining, and [3H]PK-11195 binding.
  • Evaluation of NMDA receptor involvement through co-administration with NMDA and NMDA antagonists (ifenprodil, 5, 7-dichlorokynurenic acid).

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Main Results:

  • Neomycin induced dose-dependent striatal damage, evidenced by increased gliosis.
  • Co-injection with NMDA potentiated neomycin-induced damage.
  • NMDA antagonists significantly attenuated neomycin-induced striatal injury.
  • Structurally related compounds lacking NMDA receptor activity did not cause damage.

Conclusions:

  • These findings support the hypothesis that aminoglycoside-induced ototoxicity involves NMDA receptor excitotoxicity.
  • Aminoglycosides may cause central nervous system damage, particularly in individuals with compromised blood-brain barriers.