January 4, 2010Journal of Clinical Investigation

Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents

View Full Paper

Ask AI

Bookmark

Population

Optimized adult rat-derived dorsal root ganglion neuronal expression system and computer simulations of…

Design

Preclinical

Authors

BJBrian W. JareckiUniversity of Wisconsin–Madison APAndrew D. PiekarzUniversity of North Carolina at Chapel Hill JJJames O. JacksonHunan Normal University

Discussion

Member takes

Implication

May underlie excitability in Nav channelopathies; leaves open human relevance pending validation.

Structured PICO

Population

Optimized adult rat-derived dorsal root ganglion neuronal expression system and computer simulations of nociceptive neurons and cardiac myocytes

Intervention

Introduction of disease-causing mutations in voltage-gated sodium channels (PEPD mutation in Nav1.7, PMC mutation in Nav1.4, and long-QT3/SIDS mutation in Nav1.5)

Outcome

Amplitude of resurgent sodium currents and action potential characteristics (firing frequency and broadening)surrogate

Inherited mutations in voltage-gated sodium channels, including the cardiac Nav1.5 associated with long-QT3, increase resurgent sodium currents, providing a mechanism for abnormal excitability in these channelopathies.

Cite This Study

Jarecki et al. (2010) studied this question.

synapsesocial.com/papers/6a70a248ac440176ef294cab https://doi.org/10.1172/jci40801

View Full Paper

Ask AI

Bookmark

Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider