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.
Highlights
Input from the sensory organs is required to pattern neurons into topographical maps during development
N-methyl-D-aspartateNMDA receptors (NMDARs) controls the dendritic maturation of ventroposterior medial nucleus (VPM) neurons
Suggesting that NMDARs have a role in dendritic maturation in the VPM, a developmental transcriptional analysis of VPM neurons during this time period[18] showed that expression of the NMDAR essential subunit Grin[1] increases in parallel with dendritic complexity (Fig. 1c; P = 0.016 for P0 vs. P10, Student’s t-test)
Summary
Input from the sensory organs is required to pattern neurons into topographical maps during development. 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. Severing the infraorbital nerve, which carries input from the whiskers, disrupts neuronal patterning at all relay stations of the whisker-to-cortex pathway[9, 10]. Both procedures disturb sensory mapping, the nature and specificity of the molecular/cellular processes at play in each of these conditions are poorly understood. Overexpression of Kv1.1 is sufficient to enable dendritic development in both cases, revealing that neuronal excitability is a critical a VGlut[2] GFP
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
