Selective modulation of NMDA responses by reduction and oxidation

Neuron. 1989 Mar;2(3):1257-63. doi: 10.1016/0896-6273(89)90310-3.


Electrophysiological responses to the glutamate analog N-methyl-D-aspartate (NMDA) measured in three different central neuronal preparations are subject to a novel modulatory mechanism: they are substantially potentiated after exposure to the disulfide reducing agent dithiothreitol, while oxidation with 5-5-dithiobis-2-nitrobenzoic acid decreases the magnitude of the response. Modification of the NMDA response by either oxidation or reduction does not appear to affect the pharmacological properties of the receptor-channel complex. Since we observe that the redox state of the native receptor-channel complex varies widely among neurons, an in vivo mechanism that can strongly regulate NMDA-activated functions by either reduction or oxidation may exist. In addition, these results suggest that it may be possible to design specific redox agents for characterizing the NMDA receptor-channel complex.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Aspartic Acid / analogs & derivatives*
  • Aspartic Acid / pharmacology
  • Cells, Cultured
  • Cerebral Cortex / physiology*
  • Chickens
  • Dithionitrobenzoic Acid / pharmacology
  • Dithiothreitol / pharmacology
  • Fetus
  • Membrane Potentials / drug effects
  • N-Methylaspartate
  • Neurons / drug effects
  • Neurons / physiology*
  • Oxidation-Reduction
  • Rats
  • Retina / physiology*
  • Retinal Ganglion Cells / drug effects
  • Retinal Ganglion Cells / physiology*
  • Zinc / pharmacology


  • Aspartic Acid
  • N-Methylaspartate
  • Dithionitrobenzoic Acid
  • Zinc
  • Dithiothreitol