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  NMDA receptor channels: Subunit-specific potentiation by reducing agents

Köhr, G., Eckardt, S., Lüddens, H., Monyer, H., & Seeburg, P. H. (1994). NMDA receptor channels: Subunit-specific potentiation by reducing agents. Neuron, 12(5), 1031-1040. doi:10.1016/0896-6273(94)90311-5.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0019-A91B-8 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-B1A5-1
Genre: Journal Article

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 Creators:
Köhr, Georg1, 2, 3, Author              
Eckardt, Sigrid1, Author              
Lüddens , Hartmut, Author
Monyer, Hannah1, Author              
Seeburg, Peter H.1, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Directly responsible to the Managing Director, Max Planck Institute for Medical Research, Max Planck Society, ou_persistent22              
3Georg Köhr Group, Max Planck Institute for Medical Research, Max Planck Society, ou_1497714              

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 Abstract: Sulfhydryl redox agents affect NMDA receptor activity. We investigated a putative redox site in four recombinant NMDA receptors. In 293 cells expressing NR1−NR2A channels dithiothreitol (DTT) rapidly potentiated L− glutamate−activated whole−cell currents and decreased the time course of desensitization and deactivation. Part of the current potentiation (reversible component) and all kinetic changes reversed upon washout. The remaining potentiation (persistent component) was abolished by an oxidizing agent. The N−terminal 370 residues of NR2A mediate the reversible component in chimeric NR2 subunits. In cells expressing the NR1−NR2B, −NR2C, and −NR2D channels DTT elicited only a slowly developing, persistent potentiation and increased the deactivation time course. In these, but not in NR1−NR2A, the DTT effect was rendered insensitive to reoxidation by alkylation. Reduced glutathione mimicked the DTT effects only in the NR1−NR2A receptor. Hence, molecularly distinct NMDA receptors differ profoundly in their responses to sulfhydryl redox agents

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Language(s): eng - English
 Dates: 1993-09-091994-02-222004-04-141994-05
 Publication Status: Published in print
 Pages: 10
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
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Title: Neuron
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 12 (5) Sequence Number: - Start / End Page: 1031 - 1040 Identifier: ISSN: 0896-6273
CoNE: https://pure.mpg.de/cone/journals/resource/954925560565