April 1, 1999Neurology

Defective slow inactivation of sodium channels contributes to familial periodic paralysis

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Population

Human embryonic kidney cells transiently expressing human Na channel cDNAs containing mutations associated…

Design

Preclinical

Authors

LHLawrence J. HaywardUniversity of Massachusetts Chan Medical School GSGisela M. SandovalStanford University SCStephen C. CannonBoston University

Discussion

Member takes

Implication

May differentiate Na channel mechanisms of weakness versus myotonia in HyperPP; leaves open human validation and therapeutic targeting.

Structured PICO

Population

Human embryonic kidney cells transiently expressing human Na channel cDNAs containing mutations associated with paralytic and nonparalytic phenotypes (T704M, M1592V, I693T, A1156T, V1589M)

Intervention

Expression of mutant Na channels associated with paralytic and nonparalytic phenotypes

Outcome

Extent of slow inactivation (SI) over a range of conditioning voltages, time course of entry to SI, and recovery from SIsurrogate

Slow inactivation is defective in a subset of mutant Na channels associated with episodic weakness but remains intact for mutants causing myotonia without weakness.

Cite This Study

Hayward et al. (1999) studied this question.

synapsesocial.com/papers/6a70a23675498292b70a17d2 https://doi.org/10.1212/wnl.52.7.1447

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Defective slow inactivation of sodium channels contributes to familial periodic paralysis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Defective slow inactivation of sodium channels contributes to familial periodic paralysis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider