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Next Article 
The Journal of Neuroscience, January 1, 2001, 21(1):1-9
A Calcium-Dependent Feedback Mechanism Participates in Shaping
Single NMDA Miniature EPSCs
Masashi
Umemiya1,
Nansheng
Chen2,
Lynn A.
Raymond2, and
Timothy H.
Murphy2
1 Department of Neurophysiology, Tohoku University
School of Medicine, Sendai 980-8575, Japan, and 2 Kinsmen
Laboratory Department of Physiology and Psychiatry, University of
British Columbia, Vancouver, Canada V6T 1Z3
NMDA receptors (NMDARs) are highly calcium-permeable and are
negatively regulated by intracellular calcium during prolonged exposure
to agonist. We have investigated whether calcium-mediated feedback
occurs during transient exposure to glutamate during single synaptic
events. Examination of miniature EPSCs (mEPSCs) indicated that
the decay kinetics of the NMDAR component was markedly slowed by the
intracellular perfusion of exogenous calcium buffers (BAPTA or Fluo-3).
In contrast, the AMPA receptor component of the miniature EPSC was
unaffected. Slow on-rate calcium buffers, such as EGTA, did not alter
kinetics of the NMDAR component of the mEPSC. Addition of exogenous
fast calcium buffers did not slow the decay kinetics of
glutamate-evoked currents mediated by NR1/NR2A heteromers expressed in
HEK 293 cells, suggesting that the effect we observed in neurons
may be specific to processes associated with synaptically activated
receptors. Trial-to-trial amplitude variability of miniature calcium
transients mediated by NMDARs increased with the injection of exogenous
calcium buffers, suggesting that the amplitude of synaptic calcium
transients are maintained at a rather constant level by a
calcium-mediated feedback mechanism.
Key words:
NMDA receptors; calcium; NR2A; Fluo-3; glutamate
receptor; development
Copyright © 2001 Society for Neuroscience 0270-6474/01/2111-09$05.00/0
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