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pubmed-article:2696504pubmed:abstractTextElectrophysiological 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.lld:pubmed
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pubmed-article:2696504pubmed:articleTitleSelective modulation of NMDA responses by reduction and oxidation.lld:pubmed
pubmed-article:2696504pubmed:affiliationDepartment of Neurology Research, Children's Hospital, Boston, Massachusetts 02115.lld:pubmed
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