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Depolarizing GABAergic conductances regulate the balance of excitation to inhibition in the developing retinotectal circuit in vivo

Academic Article
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Overview

authors

  • Akerman, C. J.
  • Cline, Hollis

publication date

  • May 2006

journal

  • Journal of Neuroscience  Journal

abstract

  • Neurotransmission during development regulates synaptic maturation in neural circuits, but the contribution of different neurotransmitter systems is unclear. We investigated the role of GABAA receptor-mediated Cl- conductances in the development of synaptic responses in the Xenopus visual system. Intracellular Cl- concentration ([Cl-]i) was found to be high in immature tectal neurons and then falls over a period of several weeks. GABAergic synapses are present at early stages of tectal development and, when activated by optic nerve stimulation or visual stimuli, induce sustained depolarizing Cl- conductances that facilitate retinotectal transmission by NMDA receptors. To test whether depolarizing GABAergic inputs cooperate with NMDA receptors during activity-dependent maturation of glutamatergic synapses, we prematurely reduced [Cl-]i in tectal neurons in vivo by expressing the Cl- transporter KCC2. This blocked the normal developmental increase in AMPA receptor-mediated retinotectal transmission and increased GABAergic synaptic input to tectal neurons. Therefore, depolarizing GABAergic transmission plays a pivotal role in the maturation of excitatory transmission and controls the balance of excitation and inhibition in the developing retinotectal circuit.

subject areas

  • Animals
  • Cell Membrane
  • Chloride Channels
  • Electric Conductivity
  • Excitatory Postsynaptic Potentials
  • Larva
  • Membrane Potentials
  • Neural Inhibition
  • Synaptic Transmission
  • Visual Pathways
  • Xenopus laevis
  • gamma-Aminobutyric Acid
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Research

keywords

  • GABAergic transmission
  • activity-dependent
  • glutamatergic transmission
  • intracellular chloride
  • synaptic development
  • visual system
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Identity

International Standard Serial Number (ISSN)

  • 0270-6474

Digital Object Identifier (DOI)

  • 10.1523/jneurosci.0319-06.2006

PubMed ID

  • 16687503
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Additional Document Info

start page

  • 5117

end page

  • 5130

volume

  • 26

issue

  • 19

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