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Creation of AMPA-silent synapses in the neonatal hippocampus.

Journal article
Authors Min-Yi Xiao
Pontus Wasling
Eric Hanse
Bengt Gustafsson
Published in Nature neuroscience
Volume 7
Issue 3
Pages 236-43
ISSN 1097-6256
Publication year 2004
Published at Institute of Physiology and Pharmacology, Dept of Physiology
Pages 236-43
Language en
Links dx.doi.org/10.1038/nn1196
Keywords Animals, Animals, Newborn, Calcium Signaling, drug effects, physiology, Cell Differentiation, drug effects, physiology, Cyclic AMP-Dependent Protein Kinases, antagonists & inhibitors, metabolism, Electric Stimulation, Enzyme Inhibitors, pharmacology, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, drug effects, physiology, Glutamic Acid, metabolism, Hippocampus, cytology, growth & development, metabolism, Neuronal Plasticity, drug effects, physiology, Presynaptic Terminals, drug effects, metabolism, Rats, Rats, Wistar, Receptors, AMPA, drug effects, metabolism, Receptors, N-Methyl-D-Aspartate, drug effects, metabolism, Signal Transduction, drug effects, physiology, Synapses, drug effects, metabolism, Synaptic Membranes, drug effects, metabolism, Synaptic Transmission, drug effects, physiology, Synaptic Vesicles, drug effects, metabolism
Subject categories Medical and Health Sciences

Abstract

In the developing brain, many glutamate synapses have been found to transmit only NMDA receptor-mediated signaling, that is, they are AMPA-silent. This result has been taken to suggest that glutamate synapses are initially AMPA-silent when they are formed, and that AMPA signaling is acquired through activity-dependent synaptic plasticity. The present study on CA3-CA1 synapses in the hippocampus of the neonatal rat suggests that AMPA-silent synapses are created through a form of activity-dependent silencing of AMPA signaling. We found that AMPA signaling, but not NMDA signaling, could be very rapidly silenced by presynaptic electrical stimulation at frequencies commonly used to probe synaptic function (0.05-1 Hz). Although this AMPA silencing required a rise in postsynaptic Ca(2+), it did not require activation of NMDA receptors, metabotropic glutamate receptors or voltage-gated calcium channels. The AMPA silencing, possibly explained by a removal of postsynaptic AMPA receptors, could subsequently be reversed by paired presynaptic and postsynaptic activity.

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