Dataset Information

Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly.

ABSTRACT: Voltage-gated sodium (NaV) channels, encoded by the gene para, play a critical role in the rapid processing and propagation of visual information related to collision avoidance behaviors. We investigated their localization by immunostaining the optic lobes and central brain of the grasshopper Schistocerca americana and the vinegar fly Drosophila melanogaster with an antibody that recognizes the channel peptide domain responsible for fast inactivation gating. NaV channels were detected at high density at all stages of development. In the optic lobe, they revealed stereotypically repeating fascicles consistent with the regular structure of the eye. In the central brain, major axonal tracts were strongly labeled, particularly in the grasshopper olfactory system. We used the NaV channel sequence of Drosophila to identify an ortholog in the transcriptome of Schistocerca. The grasshopper, vinegar fly, and human NaV channels exhibit a high degree of conservation at gating and ion selectivity domains. Comparison with three species evolutionarily close to Schistocerca identified splice variants of Para and their relation to those of Drosophila. The anatomical distribution of NaV channels molecularly analogous to those of humans in grasshoppers and vinegar flies provides a substrate for rapid signal propagation and visual processing in the context of visually-guided collision avoidance.

SUBMITTER: Wang H

PROVIDER: S-EPMC7073303 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly.

Wang Hongxia H Foquet Bert B Dewell Richard B RB Song Hojun H Dierick Herman A HA Gabbiani Fabrizio F

Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology 20200104 2

Voltage-gated sodium (NaV) channels, encoded by the gene para, play a critical role in the rapid processing and propagation of visual information related to collision avoidance behaviors. We investigated their localization by immunostaining the optic lobes and central brain of the grasshopper Schistocerca americana and the vinegar fly Drosophila melanogaster with an antibody that recognizes the channel peptide domain responsible for fast inactivation gating. NaV channels were detected at high de ...[more]

PMID: 31902005

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Project description:BackgroundGenetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. The mRNA splicing patterns of all four genes vary across development in the rodent brain, including mutually exclusive copies of the fifth protein-coding exon detected in the neonate (5N) and adult (5A). A second pair of mutually exclusive exons is reported in SCN8A only (18N and 18A). We aimed to quantify the expression of individual exons in the developing human brain.MethodsRNA-seq data from 783 human brain samples across development were analyzed to estimate exon-level expression. Developmental changes in exon utilization were validated by assessing intron splicing. Exon expression was also estimated in RNA-seq data from 58 developing mouse neocortical samples.ResultsIn the mature human neocortex, exon 5A is consistently expressed at least 4-fold higher than exon 5N in all four genes. For SCN2A, SCN3A, and SCN8A, a brain-wide synchronized 5N to 5A transition occurs between 24 post-conceptual weeks (2nd trimester) and 6 years of age. In mice, the equivalent 5N to 5A transition begins at or before embryonic day 15.5. In SCN8A, over 90% of transcripts in the mature human cortex include exon 18A. Early in fetal development, most transcripts include 18N or skip both 18N and 18A, with a transition to 18A inclusion occurring from 13 post-conceptual weeks to 6 months of age. No other protein-coding exons showed comparably dynamic developmental trajectories.ConclusionsExon usage in SCN1A, SCN2A, SCN3A, and SCN8A changes dramatically during human brain development. These splice isoforms, which alter the biophysical properties of the encoded channels, may account for some of the observed phenotypic differences across development and between specific variants. Manipulation of the proportion of splicing isoforms at appropriate stages of development may act as a therapeutic strategy for specific mutations or even epilepsy in general.

Dataset Information

Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly.

Publications

Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly.

Similar Datasets

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