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Modulation of low-frequency-induced synaptic depression in the developing CA3-CA1 hippocampal synapses by NMDA and metabotropic glutamate receptor activation.

Journal article
Authors Joakim Strandberg
Pontus Wasling
Bengt Gustafsson
Published in Journal of neurophysiology
Volume 101
Issue 5
Pages 2252-62
ISSN 0022-3077
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 2252-62
Language en
Keywords Animals, Animals, Newborn, Biophysics, Electric Stimulation, methods, Excitatory Amino Acid Antagonists, pharmacology, Excitatory Postsynaptic Potentials, drug effects, physiology, Hippocampus, cytology, Long-Term Synaptic Depression, drug effects, physiology, Neural Pathways, physiology, Rats, Rats, Wistar, Receptors, Metabotropic Glutamate, antagonists & inhibitors, physiology, Receptors, N-Methyl-D-Aspartate, antagonists & inhibitors, physiology, Synapses, drug effects, physiology
Subject categories Medical and Health Sciences


Brief test-pulse stimulation (0.2-0.05 Hz) of naïve (previously nonstimulated) developing hippocampal CA3-CA1 synapses leads to a substantial synaptic depression, explained by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) silencing. Using field recordings in hippocampal slices from P8 to P12 rats, we examined this depression of naïve synapses using more prolonged test-pulse stimulation as well as low-frequency (1 Hz) stimulation (LFS). We found that 900 stimuli produced depression during stimulation to approximately 40% of the naïve level independent of whether test-pulse stimulation or LFS was used. This result was also observed during combined blockade of N-methyl-d-aspartate/metabotropic glutamate receptors (NMDAR/mGluRs) although the depression was smaller (to approximately 55% of naïve level). Using separate blockade of either NMDARs or mGluRs, we found that this impairment of the depression resulted from the NMDAR, and not from the mGluR, blockade. In fact, during NMDAR blockade alone, depression was smaller even than that observed during combined blockade. We also found that mGluR blockade alone facilitated the LFS-induced depression. In conclusion, test-pulse stimulation produced as much depression as LFS when applied to naïve synapses even when allowing for NMDAR and mGluR activation. Our results seem in line with the notion that NMDARs and mGluRs may exert a bidirectional control on AMPA receptor recruitment to synapses.

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