Key result
Targeted connexin43 gene disruption in mice fails to alter cardiac Na+ channel distribution or kinetics.
Population
Neonatal ventricular myocytes isolated from Cx43 wild-type, heterozygous, and homozygous null mouse hearts
Comparison
Targeted disruption of the connexin43 (Cx43) gene vs Cx43 wild-type myocytes
Design
Preclinical
Authors
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Cx43 disruption leaves Na+ channel function unaltered in mouse myocytes; challenges direct coupling models and leaves open human relevance.
Despite the absence of Cx43 and resulting gross cardiac morphologic abnormalities, cardiac Na+ channel distribution and function remain normal in Cx43 null hearts.
Johnson et al. (1999) studied Cx43-deficient cardiac myocytes. Cx43 deficiency vs. Cx43 wild-type was evaluated on Action potential morphology, peak Na+ current, activation and inactivation kinetics, and Na+ channel protein expression and distribution. Targeted disruption of the connexin43 gene in mice did not alter cardiac Na+ channel distribution, peak Na+ current, or activation and inactivation kinetics compared to wild-type myocytes.
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