NMDA receptor redox sites: are they targets for selective neuronal protection?

Trends Pharmacol Sci. 1995 Nov;16(11):368-74. doi: 10.1016/s0165-6147(00)89077-x.

Abstract

NMDA receptors play a central role in neuronal plasticity and in several pathological situations. Transient activation of this receptor triggers long-term potentiation, whereas sustained activation leads to cell death. Evidence for control of this activity by a redox site in cell cultures, brain tissues and in recombinant NMDA receptors are discussed by Henri Gozlan and Yehezkel Ben-Ari. The characteristics of this modulation and the consequences of redox state modifications on NMDA-mediated events are examined in vitro under physiological and pathological conditions. Since metabolic disorders enhance NMDA receptor function, the redox site could constitute a new target for selectively preventing in vivo the deleterious consequences of overactivation without blocking neuronal plasticity mediated by NMDA receptors.

Publication types

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

MeSH terms

  • Alkylation
  • Animals
  • Ascorbic Acid / pharmacology
  • Brain / drug effects
  • Brain / metabolism
  • Cells, Cultured
  • Epilepsy / metabolism
  • Free Radicals
  • In Vitro Techniques
  • Ischemia / metabolism
  • Neuronal Plasticity / physiology*
  • Oxidation-Reduction
  • Receptors, N-Methyl-D-Aspartate / drug effects
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Recombinant Proteins
  • Sulfhydryl Compounds / pharmacology*
  • Sulfhydryl Compounds / therapeutic use
  • Sulfhydryl Reagents / pharmacology*
  • Sulfhydryl Reagents / therapeutic use
  • Synaptic Transmission / drug effects
  • Xenopus laevis

Substances

  • Free Radicals
  • Receptors, N-Methyl-D-Aspartate
  • Recombinant Proteins
  • Sulfhydryl Compounds
  • Sulfhydryl Reagents
  • Ascorbic Acid