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Calcium‐dependent inactivation of heteromeric NMDA receptor‐channels expressed in human embryonic kidney cells.
Author(s) -
Medina I,
Filippova N,
Charton G,
Rougeole S,
Ben-Ari Y,
Khrestchatisky M,
Bregestovski P
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020540
Subject(s) - nmda receptor , pipette , hek 293 cells , patch clamp , glutamate receptor , biophysics , microbiology and biotechnology , chemistry , receptor , hippocampal formation , depolarization , ion channel , biology , neuroscience , biochemistry
1. Whole‐cell current through heteromeric NR1‐NR2A and NR1‐NR2B subunit combinations of NMDA channels transiently expressed in human embryonic kidney cells (HEK 293) were studied using the patch‐clamp technique. 2. With 4 mM Mg‐ATP in the internal pipette solution, the responses of cells expressing NR1‐NR2A channels to glutamate application gradually decreased, reaching 50% of control during the first 20 min of recording. This process was accompanied by acceleration of desensitization. 3. Conditioning (5‐15 s) applications of glutamate (100 microM) induced a transient inactivation of NR1‐NR2A and NR1‐NR2B channels (20‐40%) with a slow time course of recovery (tau r = 10‐60 s). Both the degree of inactivation and the time constant of recovery increased with the duration of conditioning applications of glutamate, and with an elevation of Ca2+ in the external solution. 4. These results show that both NR1‐NR2A and NR1‐NR2B recombinant NMDA receptor‐channels expressed in HEK 293 cells can be transiently inhibited by Ca2+ ions in a similar way to that described for hippocampal neurones.