Fast interaction between AMPA and NMDA receptors by intracellular calcium
Suppression of NMDA receptor (NMDAR)-mediated currents by intracellular Ca2+ has been described as a negative feedback loop in NMDAR modulation. In the time scale of tenths of milliseconds the depth of the suppression does not depend on the Ca2+ source. It may be caused by Ca2+ influx through voltag...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
28 September 2016
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| In: |
Cell calcium
Year: 2016, Volume: 60, Issue: 6, Pages: 407-414 |
| ISSN: | 1532-1991 |
| DOI: | 10.1016/j.ceca.2016.09.005 |
| Online Access: | Resolving-System, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.ceca.2016.09.005 Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0143416016301038 
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| Author Notes: | Andrei Rozov, Nail Burnashev |
MARC
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| 520 | |a Suppression of NMDA receptor (NMDAR)-mediated currents by intracellular Ca2+ has been described as a negative feedback loop in NMDAR modulation. In the time scale of tenths of milliseconds the depth of the suppression does not depend on the Ca2+ source. It may be caused by Ca2+ influx through voltage-gated calcium channels, NMDAR channels or release from intracellular stores. However, NMDARs are often co-expressed in synapses with Ca2+-permeable AMPA receptors (AMPARs). Due to significant differences in activation kinetics between these two types of glutamate receptors (GluRs), Ca2+ entry through AMPARs precedes full activation of NMDARs, and therefore, might have an impact on the amplitude of NMDAR-mediated currents. The study of Ca2+-mediated crosstalk between AMPAR and NMDAR in native synapses is challenging due to high NMDAR Ca2+ permeability. Therefore, recombinant Ca2+-permeable AMPAR and Ca2+-impermeable NMDAR mutant channels were co-expressed in HEK 293 cells to examine their interaction. An AMPAR-mediated increase in intracellular Ca2+ concentration ([Ca2+]i) reversibly reduced the size of NMDAR-mediated whole-cell currents. The time course of the NMDAR channel inactivation and recovery from inactivation followed the time course of the [Ca2+]i transient. When brief (1ms) pulses of glutamate were applied to outside-out patches, the degree of NMDAR inactivation increased with the increase in charge carried by the currents through co-activated AMPARs. However, AMPAR-mediated NMDAR inactivation was abolished in the presence of intracellular fast Ca2+ buffer BAPTA or in Ca2+-free extracellular solution. We conclude that Ca2+ entering through AMPARs inactivates co-localized NMDARs in the time range of excitatory postsynaptic currents. | ||
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