![]() ![]() Cell type-specific three-dimensional structure of thalamocortical circuits in a column of rat vibrissal cortex. Reconstruction and simulation of neocortical microcircuitry. NeuroMorpho.Org: a central resource for neuronal morphologies. Neuronal cell-type classification: challenges, opportunities and the path forward. Together, our study provides a comprehensive structural repertoire for the reconstruction and analysis of PFC neural network. Finally, integrative dendrite–axon analysis uncovered the organization of potential intra-column, inter-hemispheric and inter-column connectivity among projection neuron types in PFC. ![]() Furthermore, correspondence analysis among dendrites, local axons and long-range axons revealed coherent morphological changes associated with electrophysiological phenotypes. We uncovered 24 morphologically distinguishable dendrite subtypes in 1,515 pyramidal projection neurons and 405 atypical pyramidal projection neurons and spiny stellate neurons with unique axon projection patterns. We identified morphological variations of somata, dendrites and axons across laminar layers and PFC subregions and the general rules of somatodendritic scaling with cytoarchitecture. Here we report the complete dendrite and axon morphology of nearly 2,000 neurons in mouse prefrontal cortex (PFC). Published by Elsevier B.V.The structures of dendrites and axons form the basis for the connectivity of neural network, but their precise relationship at single-neuron level remains unclear. ![]() We propose that early therapeutic strategies in DS could help minimize the effect of sodium channelopathies, beyond the impact of overt seizures, and therefore achieve better long-term treatment outcomes.Īxon architecture Brain structure Dravet syndrome Epilepsy Genetic disorders Neurodevelopment.Ĭopyright © 2020. The pilot study provides a basis for future meta-analysis that will enable robust estimates of the effects of the sodium channelopathy on axon architecture. The data has indicated, in the absence of behavioral seizures, factors that governed a shift toward small calibre axons at P16 have persisted in adult Scn1a heterozygote KO corpus callosum. Qualitative analysis also shows micro-features marking altered myelination at P16 in the DS model, with myelin out-folding and myelin debris within phagocytic cells. Pilot data for Scn1a heterozygote KO mice demonstrate the average axon caliber was reduced in developing and adult mice. Trainable machine learning algorithms were used to examine electron microscopy images of ~400 myelinated axons per animal, per genotype, including myelinated axon cross-section area, frequency distribution and g-ratios. Morphometric analyses of axons within the corpus callosum were completed at P16 and P50 in Scn1a heterozygote KO male mice and their age-matched wild-type littermates. We have investigated whether the sodium channelopathy may result in structural changes in the DS model independent of seizures. This mutation causes a loss-of-function in inhibitory neurons, initiating seizure onset. A majority of DS patients have an SCN1A heterozygous gene mutation. Recurrent severe seizures begin in infancy and co-morbidities follow, including developmental delay, cognitive and behavioral dysfunction. Dravet Syndrome (DS) is a genetic neurodevelopmental disease. ![]()
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