Abstract
Redox phenomena seem to modulate activity of the N-methyl-D-aspartate receptor. Some reductants (ascorbate, hydroquinone) inhibit, while others (dithiothreitol, mercaptoethanol, penicillamine) potentiate NMDA receptor function. Ascorbate inhibits binding of [3H]glutamate and [3H]thienylcycohexylpiperidine to the NMDA receptor complex, and impedes NMDA-gated currents in isolated neurons; dithiothreitol-like reductants enhance NMDA-induced currents. The ability of reductants to alter function of the NMDA receptor is abolished by oxidation.
MeSH terms
-
Animals
-
Ascorbic Acid / pharmacology*
-
Cerebral Cortex / cytology
-
Dithiothreitol / pharmacology
-
Electrophysiology
-
In Vitro Techniques
-
Ion Channel Gating / drug effects
-
Kainic Acid / metabolism
-
Kinetics
-
Mercaptoethanol / pharmacology
-
N-Methylaspartate / metabolism
-
Neurons / drug effects
-
Oxidation-Reduction
-
Penicillamine / pharmacology
-
Quisqualic Acid / metabolism
-
Rats
-
Receptors, Glutamate
-
Receptors, N-Methyl-D-Aspartate / drug effects
-
Receptors, N-Methyl-D-Aspartate / metabolism*
-
Receptors, Neurotransmitter / drug effects
Substances
-
Receptors, Glutamate
-
Receptors, N-Methyl-D-Aspartate
-
Receptors, Neurotransmitter
-
Mercaptoethanol
-
N-Methylaspartate
-
Quisqualic Acid
-
Penicillamine
-
Ascorbic Acid
-
Kainic Acid
-
Dithiothreitol