Medical Journals

Activation of Presynaptic Gaba(A) Receptors Induces Glutamate Release from Parallel Fiber Synapses.

Authors:
  • Stell Brandon M
  • Rostaing Philippe
  • Triller Antoine
  • Marty Alain

From: Laboratoire de Physiologie Cérébrale, Unité de Formation et de Recherche Biomédicale, Université Paris Descartes, 75006 Paris, France. brandon.stell@univ-paris5.fr

The Journal of neuroscience : the official journal of the Society for Neuroscience

  • Publish Date: Aug 2007
  • ISSN: 1529-2401
  • Volume: 27
  • Issue: 34
  • Pages: 9022-31
  • Medium: Internet
  • Language: English
  • Citation (JAMA): Stell Brandon M, Rostaing Philippe, Triller Antoine, et al. Activation of Presynaptic Gaba(A) Receptors Induces Glutamate Release from Parallel Fiber Synapses.. J. Neurosci. Aug 2007;27:9022-31

Abstract

The parallel fibers relay information coming into the cerebellar cortex from the mossy fibers, and they form synapses with molecular layer interneurons (MLIs) and Purkinje cells. Here we show that activation of ionotropic GABA receptors (GABA(A)Rs) induces glutamate release from parallel fibers onto both MLIs and Purkinje cells. These GABA-induced EPSCs have kinetics and amplitudes identical to random spontaneous currents (sEPSCs), but, unlike sEPSCs, they occur in bursts of between one and five successive events. The variation in amplitude of events within bursts is significantly less than the variation of all sEPSC amplitudes, suggesting that the bursts result from repetitive activation of single presynaptic fibers. Electron microscopy of immunogold-labeled alpha-1 subunits revealed GABA(A)Rs on parallel fiber terminals. We suggest that the activation of these receptors underlies the increased amplitude of parallel fiber-evoked Purkinje cell EPSCs seen with application of exogenous GABA or after the release of GABA from local interneurons. These results occur only when molecular layer GABA(A)Rs are activated, and the effects are abolished when the receptors are blocked by the GABA(A)R antagonist gabazine (5 microM). From these data, we conclude that GABA(A)Rs located on parallel fibers depolarize parallel fiber terminals beyond the threshold for Na+ channel activation and thereby induce glutamate release onto MLIs and Purkinje cells.

Mesh Headings (Keywords): Animals, Animals, Newborn, Cerebellum, Electric Stimulation, Excitatory Postsynaptic Potentials, GABA Agonists, GABA Antagonists, Glutamic Acid, Interneurons, Microscopy, Electron, Transmission, Muscimol, Patch-Clamp Techniques, Phosphinic Acids, Presynaptic Terminals, Propanolamines, Purkinje Cells, Rats, Receptors, GABA-A, Synapses, Time Factors, gamma-Aminobutyric Acid


Check for Full Text / PubMed Unique Identifier (PMID): 17715339


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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