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.Sensory input and neuronal activity are crucial for proper morphological development of neurons. Here, Frangeul and colleagues show that membrane excitability is a critical component of dendritic development in mouse somatosensory thalamocortical neurons.
Input-dependent regulation of excitability controls dendritic maturation in somatosensory thalamocortical neurons
Laura Frangeul,Vassilis Kehayas,J. Sanchez-Mut,Sabine Fièvre,K. Krishna-K,Gabrielle Pouchelon,Ludovic Telley,C. Bellone,A. Holtmaat,Johannes Gräff,J. D. Macklis,D. Jabaudon
Published 2017 in Nature Communications
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- Publication year
2017
- Venue
Nature Communications
- Publication date
2017-12-08
- Fields of study
Biology, Medicine
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Semantic Scholar, PubMed
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