![]() Watching developing neurons under the time-lapse microscope as they pick one dendrite among many to crown as the axon is a source of wonderment for many neurobiologists. But using better imaging techniques the researchers now found that it is the basal dendrites below where the AcDs are more likely to be found. In other words, the upper regions of the extended cell. It had been previously shown by other researchers that around 5% of CA1 pyramidal cells had axons shooting out of their apical dendrites. The researchers had a look at the other parts of the hippocampus as well and found that about a quarter of the pyramidal cells there had AcDs too. While it probably shouldn't be applied to situations where the majority is only 51 percent, if 20 out of the 36 cells you checked on had AcDs, it's probably at least a trend. Many would argue about what percent of something the word "most" actually means. Rather than mere quirk or curiousity the axon carrying dendrite, or AcD as the authors call it, is found on most neurons-at least among pyramidal cells in the CA1 area of the mouse hippocampus. ![]() A paper recently published in Neuron now suggests that minimizing this fundamental neural character has been a mistake. The existence of these anomalies is an inconvenient truth for all neuron modelers and typically they choose to ignore them. Certain interneurons, dopaminergic cells, or neuroendicrine cells for example, have been shown to grow their axon out from a lucky dendrite instead of the soma. There have always been exceptions to this neat and tidy picture of a neuron. The electrical energy of these signals is generally believed to be integrated at the cell body and converted into pulses at the axon initial segment (this is the region where the axon sprouts, the AIS). (Medical Xpress)-The well-behaved neuron receives signals through its many dendrites to generate spikes on a single axon. This study provides the first case of microdeletion limited to the SCN1A 5' promoter region with the coding sequence preserved, and indicates the critical involvement of this upstream region in the molecular pathology of Dravet syndrome.Creating of the axon. One patient with symptomatic focal epilepsy also showed a deletion in the coding region. We also identified four patients with deletions/duplication in the coding region. Among 71 Dravet syndrome patients, we found two patients with heterozygous microdeletions removing the 5' noncoding exons and regions with promoter activity but not affecting the coding exons. Using multiplex ligation-dependent probe amplification (MLPA) assays with probes for the 5' noncoding exons, their upstream regions, and all coding exons of SCN1A, we investigated 130 epileptic patients who did not show any SCN1A mutations by sequence analysis of all coding exons and exon-intron boundaries. These two major promoters were simultaneously active in various brain regions and in most neurons. Here we investigated the upstream regions of the SCN1A 5' noncoding exons and found two major regions with promoter activity. Mutations involving the voltage-gated sodium channel alpha(I) gene SCN1A are major genetic causes of childhood epileptic disorders, as typified by Dravet syndrome.
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