Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Home
Search
Quick Search
Advanced
Fulltext
Browse
Collections
Persons
My eDoc
Session History
Login
Name:
Password:
Documentation
Help
Support Wiki
Direct access to
document ID:


          Institute: MPI für medizinische Forschung     Collection: Abteilung Molekulare Neurobiologie     Display Documents



ID: 22431.0, MPI für medizinische Forschung / Abteilung Molekulare Neurobiologie
NMDA receptor channels: subtype specific potentiation by reducing agents
Translation of Title:NMDA receptor channels: subtype specific potentiation by reducing agents
Authors:Köhr, Georg; Eckardt, Sigrid; Lüddens, H.; Monyer, Hannah; Seeburg, Peter H.
Language:English
Date of Publication (YYYY-MM-DD):1994-05
Title of Journal:Neuron
Journal Abbrev.:Neuron
Volume:12
Issue / Number:5
Start Page:1031
End Page:1040
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description: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.
External Publication Status:published
Document Type:Article
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie/
Identifiers:URI:http://www.neuron.org/cgi/content/abstract/12/5/10... [Abstract]
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.