J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Volume 543, Number 1, 23-33, August 15, 2002 DOI: 10.1113/jphysiol.2002.020321
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
543/1/23    most recent
2002.020321v1
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bai, D.
Right arrow Articles by Roder, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bai, D.
Right arrow Articles by Roder, J. C.
Journal of Physiology (2002), 543.1, pp. 23-33
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.020321

Non-ionotropic cross-talk between AMPA and NMDA receptors in rodent hippocampal neurones

Donglin Bai*, Robert U. Muller†‡ and John C. Roder*

*Samuel Lunenfeld Research Institute, Mount Sinai Hospital and Institute of Medical Science, University of Toronto, 600 University Avenue, Toronto, Ontario, Canada M5G 1X5, †Department of Physiology, SUNY Health Science Center Brooklyn, 450 Clarkson Avenue, Brooklyn, NY 11203, USA and ‡MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, University Walk, Bristol BS8 1TD, UK

Many fast excitatory synapses in the hippocampus are enriched with both AMPARs (alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate receptors) and NMDARs (N-methyl-D-aspartate receptors). Their proximity allows them to be activated simultaneously by the same neurotransmitter, L-glutamate. Activation of AMPARs leads to influx of sodium and calcium ions, which can increase or decrease NMDAR activity through sodium concentration-dependent cascades or a calcium-calmodulin-dependent inactivation process, respectively. Here we provide evidence that the activation of AMPARs inhibits NMDARs through a non-ionotropic mechanism. NMDA-induced current in isolated rat CA1 hippocampal cells and nucleated patches of cultured mouse hippocampal neurones decreased when AMPARs were activated. Conversely, when AMPARs were blocked, the NMDA component of glutamate-induced current increased. The inhibitory action of AMPAR activation on NMDAR-mediated current depends upon the open state of AMPA channels and rapidly diminishes after deactivation of AMPARs. The inhibitory action was independent of membrane voltage, univalent cation fluxes and calcium influx. The AMPA-NMDA cross-inhibition also occurred in evoked synaptic current in CA1 neurones from intact mouse hippocampal slices. This cross-talk may play a role in preventing overexcitation during bursting activities in the hippocampus.



This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
M. E. Pamenter, D. S.-H. Shin, and L. T. Buck
AMPA receptors undergo channel arrest in the anoxic turtle cortex
Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R606 - R613.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 The Physiological Society.