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Kcc2 expression promotes the termination of cortical interneuron migration in a voltage-sensitive calcium-dependent manner

Academic Article
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Overview

authors

  • Bortone, D.
  • Polleux, Franck

publication date

  • 2009

journal

  • Neuron  Journal

abstract

  • The molecular mechanisms controlling the termination of cortical interneuron migration are unknown. Here, we demonstrate that, prior to synaptogenesis, migrating interneurons change their responsiveness to ambient GABA from a motogenic to a stop signal. We found that, during migration into the cortex, ambient GABA and glutamate initially stimulate the motility of interneurons through both GABA(A) and AMPA/NMDA receptor activation. Once in the cortex, upregulation of the potassium-chloride cotransporter KCC2 is both necessary and sufficient to reduce interneuron motility through its ability to reduce membrane potential upon GABA(A) receptor activation, which decreases the frequency of spontaneous intracellular calcium transients initiated by L-type voltage-sensitive calcium channel (VSCC) activation. Our results suggest a mechanism whereby migrating interneurons determine the relative density of surrounding interneurons and principal cells through their ability to sense the combined extracellular levels of ambient glutamate and GABA once GABA(A) receptor activation becomes hyperpolarizing.

subject areas

  • Age Factors
  • Animals
  • Animals, Newborn
  • Bicuculline
  • Calcium
  • Calcium Channel Blockers
  • Calcium Channels, L-Type
  • Cell Movement
  • Cerebral Cortex
  • Electroporation
  • Embryo, Mammalian
  • Female
  • GABA Agents
  • Gene Expression Regulation
  • Glutamic Acid
  • Green Fluorescent Proteins
  • Homeodomain Proteins
  • Interneurons
  • LIM-Homeodomain Proteins
  • Membrane Potentials
  • Mice
  • Mice, Inbred BALB C
  • Mice, Transgenic
  • Microtubule-Associated Proteins
  • Models, Biological
  • Muscimol
  • Nerve Tissue Proteins
  • Nifedipine
  • Organ Culture Techniques
  • Pregnancy
  • Quinoxalines
  • RNA, Small Interfering
  • Receptors, N-Methyl-D-Aspartate
  • Sequence Deletion
  • Symporters
  • Transcription Factors
  • Valine
  • gamma-Aminobutyric Acid
  • omega-Conotoxin GVIA
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Identity

PubMed Central ID

  • PMC3314167

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/j.neuron.2009.01.034

PubMed ID

  • 19376067
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Additional Document Info

start page

  • 53

end page

  • 71

volume

  • 62

issue

  • 1

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