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Record W3118725299 · doi:10.1113/jp280838

R1617Q epilepsy mutation slows Na<sub>V</sub>1.6 sodium channel inactivation and increases the persistent current and neuronal firing

2021· article· en· W3118725299 on OpenAlexafffund
Hugo Poulin, Mohamed Chahine

Bibliographic record

VenueThe Journal of Physiology · 2021
Typearticle
Languageen
FieldNeuroscience
TopicNeuroscience and Neuropharmacology Research
Canadian institutionsUniversité Laval
FundersCanadian Institutes of Health Research
KeywordsSodium channelRiluzoleEpilepsyChemistryMutationTetrodotoxinNeurosciencePatch clampMutantSodium channel blockerBiophysicsSodiumPharmacologyElectrophysiologyInternal medicineGlutamate receptorBiologyBiochemistryMedicineReceptor

Abstract

fetched live from OpenAlex

Key points A human NaV1.6 construct was established to study the biophysical consequences of the R1617Q mutation on NaV1.6 identified in patients with unclassified epileptic encephalopathy and severe intellectual disability. The R1617Q mutation disrupts the inactivation process of the channel, and more specifically, slows the current decay, increases the persistent sodium current that was blocked by tetrodotoxin and riluzole, and disrupts the inactivation voltage‐dependence and increases the kinetics of recovery. In native hippocampal neurons, the R1617Q mutation exhibited a significant increase in action potentials triggered in response to stimulation and a significant increase in the number of neurons that exhibited spontaneous activity compared to neurons expressing WT channels that were inhibited by riluzole. The abnormally persistent current activity caused by the disruption of the channel inactivation process in NaV1.6/R1617Q may result in epileptic encephalopathy in patients. Abstract The voltage‐gated sodium channel NaV1.6 is the most abundantly expressed sodium channel isoform in the central nervous system. It plays a critical role in saltatory and continuous conduction. Although over 40 NaV1.6 mutations have been linked to epileptic encephalopathy, only a few have been functionally analysed. In the present study, we characterized a NaV1.6 mutation (R1617Q) identified in patients with epileptic encephalopathy and intellectual disability. R1617Q substitutes an arginine for a glutamine in the S4 segment of domain IV, which plays a major role in coupling the activation and inactivation of sodium channels. We used patch‐clamp to show that R1617Q is a gain‐of‐function mutation. It is typified by slower inactivation kinetics and a loss of inactivation of voltage‐dependence, which result in a 2.5‐fold increase in the window current. In addition, sodium currents exhibited an enhanced rate of recovery from inactivation, most likely due to the destabilization of the inactivation state. The alterations in the fast inactivation caused a significant increase in the persistent sodium current. Overexpression of R1617Q in rat hippocampal neurons resulted in an increase in action potential firing activity that was inhibited by riluzole, consistent with the gain‐of‐function observed. We conclude that the R1617Q mutation causes neuronal hyperexcitability and may result in epileptic encephalopathy.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.052
GPT teacher head0.315
Teacher spread0.263 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations11
Published2021
Admission routes2
Has abstractyes

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