Key result
Cx43 ablation cuts intercellular electrical conductance ~70% and reduces peak sodium currents in atrial myocytes.
Why the study?
Remodelling and regional gradients in connexin expression are thought to contribute to atrial electrical dysfunction and atrial fibrillation, but the interaction between Cx43, Cx40, Cx45, and sodium current in atrial myocytes is not fully understood.
Population
Engineered pairs of atrial myocytes from wild-type and Cx43-ablated mice (1 day before birth, 3-5 days in culture)
Comparison
Cx43 genetic ablation (Cx43-/-) vs wild-type (Cx43+/+)
Design
Preclinical experimental study using microcontact printing and voltage clamp techniques
Authors
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Cx43 ablation effects on atrial coupling and I(Na) in mouse pairs warrant caution; leaves open role in human AF remodeling.
Genetic ablation of Cx43 in foetal atrial myocytes decreases electrical coupling, partner connexins, and sodium current, highlighting complex interactions in intercalated discs relevant to arrhythmogenesis.
Desplantez et al. (2012) studied Atrial electrical dysfunction. Genetic ablation of Cx43 vs. Wild-type mice (Cx43+/+) was evaluated on Intercellular electrical conductance and peak inward Na current. Genetic ablation of Cx43 in foetal atrial myocytes decreased intercellular electrical conductance from 80 nS to 24 nS and peak sodium current from -350 pA/pF to -154 pA/pF.
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