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Non-hyperpolarizing GABAB receptor activation regulates neuronal migration and neurite growth and specification by cAMP/LKB1

Author

Listed:
  • Guillaume Bony

    (Istituto Italiano di Tecnologia, Via Morego)

  • Joanna Szczurkowska

    (Istituto Italiano di Tecnologia, Via Morego)

  • Ilaria Tamagno

    (Istituto Italiano di Tecnologia, Via Morego)

  • Maya Shelly

    (State University of New York)

  • Andrea Contestabile

    (Istituto Italiano di Tecnologia, Via Morego)

  • Laura Cancedda

    (Istituto Italiano di Tecnologia, Via Morego)

Abstract

γ-Aminobutyric acid is the principal inhibitory neurotransmitter in adults, acting through ionotropic chloride-permeable GABAA receptors (GABAARs), and metabotropic GABABRs coupled to calcium or potassium channels, and cyclic AMP signalling. During early development, γ-aminobutyric acid is the main neurotransmitter and is not hyperpolarizing, as GABAAR activation is depolarizing while GABABRs lack coupling to potassium channels. Despite extensive knowledge on GABAARs as key factors in neuronal development, the role of GABABRs remains unclear. Here we address GABABR function during rat cortical development by in utero knockdown (short interfering RNA) of GABABR in pyramidal-neuron progenitors. GABABR short interfering RNA impairs neuronal migration and axon/dendrite morphological maturation by disrupting cyclic AMP signalling. Furthermore, GABABR activation reduces cyclic AMP-dependent phosphorylation of LKB1, a kinase involved in neuronal polarization, and rescues LKB1 overexpression-induced defects in cortical development. Thus, non-hyperpolarizing activation of GABABRs during development promotes neuronal migration and morphological maturation by cyclic AMP/LKB1 signalling.

Suggested Citation

  • Guillaume Bony & Joanna Szczurkowska & Ilaria Tamagno & Maya Shelly & Andrea Contestabile & Laura Cancedda, 2013. "Non-hyperpolarizing GABAB receptor activation regulates neuronal migration and neurite growth and specification by cAMP/LKB1," Nature Communications, Nature, vol. 4(1), pages 1-15, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2820
    DOI: 10.1038/ncomms2820
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