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The Novel Activity of Carbamazepine as an Activation Modulator Extends from Na_V1.7 Mutations to the Na_V1.8-S242T Mutant Channel from a Patient with Painful Diabetic Neuropathy.

ABSTRACT: Neuropathic pain in patients carrying sodium channel gain-of-function mutations is generally refractory to pharmacotherapy. However, we have shown that pretreatment of cells with clinically achievable concentration of carbamazepine (CBZ; 30 μM) depolarizes the voltage dependence of activation in some Na_V1.7 mutations such as S241T, a novel CBZ mode of action of this drug. CBZ reduces the excitability of dorsal root ganglion (DRG) neurons expressing Na_V1.7-S241T mutant channels, and individuals carrying the S241T mutation respond to treatment with CBZ. Whether the novel activation-modulating activity of CBZ is specific to Na_V1.7, and whether this pharmacogenomic approach can be extended to other sodium channel subtypes, are not known. We report here t

SUBMITTER: Han C

PROVIDER: S-EPMC7501587 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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The Novel Activity of Carbamazepine as an Activation Modulator Extends from Na_V1.7 Mutations to the Na_V1.8-S242T Mutant Channel from a Patient with Painful Diabetic Neuropathy.

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Dataset Information

The Novel Activity of Carbamazepine as an Activation Modulator Extends from NaV1.7 Mutations to the NaV1.8-S242T Mutant Channel from a Patient with Painful Diabetic Neuropathy.

OmicsDI is part of the ELIXIR infrastructure

Tweets

The Novel Activity of Carbamazepine as an Activation Modulator Extends from Na_V1.7 Mutations to the Na_V1.8-S242T Mutant Channel from a Patient with Painful Diabetic Neuropathy.