Input-dependent regulation of excitability controls dendritic maturation in somatosensory thalamocortical neurons

Laura Frangeul, Vassilis Kehayas, Jose V. Sanchez-Mut, Sabine Fièvre, K. Krishna-K, Gabrielle Pouchelon, Ludovic Telley, Camilla Bellone, Anthony Holtmaat, Johannes Gräff, Jeffrey D. Macklis and Denis Jabaudon ()
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Laura Frangeul: University of Geneva
Vassilis Kehayas: University of Geneva
Jose V. Sanchez-Mut: Brain Mind Institute, School of Life Science, Ecole Polytechnique Fédérale de Lausanne
Sabine Fièvre: University of Geneva
K. Krishna-K: University of Geneva
Gabrielle Pouchelon: University of Geneva
Ludovic Telley: University of Geneva
Camilla Bellone: University of Geneva
Anthony Holtmaat: University of Geneva
Johannes Gräff: Brain Mind Institute, School of Life Science, Ecole Polytechnique Fédérale de Lausanne
Jeffrey D. Macklis: Center for Brain Science, Harvard University
Denis Jabaudon: University of Geneva

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract Input from the sensory organs is required to pattern neurons into topographical maps during development. Dendritic complexity critically determines this patterning process; yet, how signals from the periphery act to control dendritic maturation is unclear. Here, using genetic and surgical manipulations of sensory input in mouse somatosensory thalamocortical neurons, we show that membrane excitability is a critical component of dendritic development. Using a combination of genetic approaches, we find that ablation of N-methyl-d-aspartate (NMDA) receptors during postnatal development leads to epigenetic repression of Kv1.1-type potassium channels, increased excitability, and impaired dendritic maturation. Lesions to whisker input pathways had similar effects. Overexpression of Kv1.1 was sufficient to enable dendritic maturation in the absence of sensory input. Thus, Kv1.1 acts to tune neuronal excitability and maintain it within a physiological range, allowing dendritic maturation to proceed. Together, these results reveal an input-dependent control over neuronal excitability and dendritic complexity in the development and plasticity of sensory pathways.

Date: 2017
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DOI: 10.1038/s41467-017-02172-1

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