![]() 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). In addition to epilepsy, hemiplegic migraine, ASD, sudden death, and arthrogryposis multiplex congenital can also be caused by mutations of SCN1A.ĭravet syndrome GEFS+ SCN1A autism spectrum disorder migraine.Ĭopyright © 2021 Ding, Li, Tian, Wang, Guo, Wang, Li, Wang and Sun.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. Conclusion: Aside from DS, SCN1A also causes other epileptic encephalopathies, such as GEFS+, Doose syndrome, EIMFS, West syndrome, LGS, Rett syndrome, and NEE. Overall, 303 studies on DS, 93 on GEFS+, three on Doose syndrome, nine on the epilepsy of infancy with migrating focal seizures (EIMFS), six on the West syndrome, two on the Lennox-Gastaut syndrome (LGS), one on the Rett syndrome, seven on the nonsyndromic epileptic encephalopathy (NEE), 19 on hemiplegia migraine, six on autism spectrum disorder (ASD), two on nonepileptic SCN1A-related sudden deaths, and two on the arthrogryposis multiplex congenital were included. A total of 453 studies published between 20 met the final inclusion criteria. Results: The PubMed and SCOPUS search yielded 2,889 items. The results reported by each study were summarized narratively. Methods: We searched PubMed and SCOPUS for all the published cases related to gene mutations of SCN1A until October 20, 2021. Objective: The aim of this study is to systematically review the literature associated with SCN1A and other non-DS-related disorders. Although it is known that SCN1A is the main cause of DS and genetic epilepsy with febrile seizures plus (GEFS+), there is a dearth of information on the other related diseases caused by mutations of SCN1A. More than 1,800 mutations have been identified in SCN1A. About 80% of SCN1A gene mutations cause Dravet syndrome (DS), which is a severe and catastrophic epileptic encephalopathy. Background: SCN1A is one of the most common epilepsy genes. ![]()
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