Medical Journals

Functional Maturation of Ca1 Synapses Involves Activity-dependent Loss of Tonic Kainate Receptor-mediated Inhibition of Glutamate Release.

Authors:
  • Lauri Sari E
  • Vesikansa Aino
  • SegerstrÃ¥le Mikael
  • Collingridge Graham L
  • Isaac John T R
  • Taira Tomi

From: Neuroscience Center and Department of Bio- and Environmental Sciences, P.O. Box 65 (Viikinkaari 1), 00014 University of Helsinki, Finland.

Neuron

  • Publish Date: May 2006
  • ISSN: 0896-6273
  • Volume: 50
  • Issue: 3
  • Pages: 415-29
  • Medium: Print
  • Language: English
  • Citation (JAMA): Lauri Sari E, Vesikansa Aino, SegerstrÃ¥le Mikael, et al. Functional Maturation of Ca1 Synapses Involves Activity-dependent Loss of Tonic Kainate Receptor-mediated Inhibition of Glutamate Release.. Neuron May 2006;50:415-29

Abstract

Early in development, excitatory synapses transmit with low efficacy, one mechanism for which is a low probability of transmitter release (Pr). However, little is known about the developmental mechanisms that control activity-dependent maturation of the presynaptic release. Here, we show that during early development, transmission at CA3-CA1 synapses is regulated by a high-affinity, G protein-dependent kainate receptor (KAR), which is endogenously activated by ambient glutamate. By tonically depressing glutamate release, this mechanism sets the dynamic properties of neonatal inputs to favor transmission during high frequency bursts of activity, typical for developing neuronal networks. In response to induction of LTP, the tonic activation of KAR is rapidly down regulated, causing an increase in Pr and profoundly changing the dynamic properties of transmission. Early development of the glutamatergic connectivity thus involves an activity-dependent loss of presynaptic KAR function producing maturation in the mode of excitatory transmission from CA3 to CA1.

Mesh Headings (Keywords): Action Potentials, Aging, Animals, Cell Differentiation, Down-Regulation, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, Glutamic Acid, Hippocampus, Long-Term Potentiation, Neural Inhibition, Neural Pathways, Organ Culture Techniques, Presynaptic Terminals, Rats, Receptors, G-Protein-Coupled, Receptors, Kainic Acid, Synaptic Transmission


Check for Full Text / PubMed Unique Identifier (PMID): 16675396


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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