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Regulation of fin regeneration by a voltage-gated sodium channel

ABSTRACT: Regulation of fin regeneration by a voltage-gated sodium channel

PROVIDER: PRJNA775662 | ENA |

REPOSITORIES: ENA

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Regulation of fin regeneration by a voltage-gated sodium channel

Project description:We compare the brain and fin RNA-seq profiles of wild-type and scn8ab mutant zebrafish, which exhibit locomotion and fin regeneration defects.

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Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

Project description:Scn2a encodes voltage-gated sodium channel NaV1.2, a main mediator of neuronal action potential firing. The current paradigm suggests that NaV1.2 gain-of-function variants enhance neuronal excitability resulting in epilepsy, whereas NaV1.2 deficiency impairs excitability contributing to autism. This paradigm, however, does not explain why 20~30% of patients with NaV1.2 deficiency still develop seizures. Here we report a counterintuitive finding that severe NaV1.2 deficiency results in increased neuronal excitability. Using a unique NaV1.2-deficient mouse model, we found enhanced intrinsic excitabilities of principal neurons in the prefrontal cortex and striatum, brain regions known to be involved in Scn2a-related seizures. This increased excitability is autonomous, and is reversible by the genetic restoration of Scn2a expression in adult mice. RNA-sequencing revealed that the downregulation of multiple potassium channels including KV1.1, and KV channel openers alleviated hyperexcitability of NaV1.2-deficient neurons. This unexpected neuronal hyperexcitability may serve as a cellular basis underlying NaV1.2 deficiency-related seizures.

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Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

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Project description:We investigated the effects of nimodipine, a L-type voltage-gated calcium channel antagonist, on the expression profile of myelin genes in the oligodendrocyte precursor cell (OPC) line Oli-Neu. We performed gene expression profiling analysis using data obtained from RNA-seq of four biological replicates for treatment and four replicates for control condition.

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Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

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Voltage-gated sodium channel (VGSC) beta1 subunit-intracellular domain (Beta1-ICD) overexpression in Chinese hamster lung cells

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