Key result
Site-3 toxins reduced maximal gating charge by 33% in rat skeletal muscle and by 31% in human heart sodium channels, while slowing the decay of sodium current in both channel types.
Faster kinetics in rat skeletal muscle channels compared with human heart channels may arise from inherently faster rate transitions rather than major differences in voltage dependence.
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Site-3 toxin effects on NaV gating appear conserved across species; hypothesis-generating for cardiac applications pending in vivo validation.
Sheets et al. (1999) studied this question. Site-3 toxins (Anthopleurin A and Anthopleurin B) vs. Control solutions was evaluated on Sodium channel ionic current (INa) and gating current (Ig). Site-3 toxins reduced maximal gating charge by 33% in rat skeletal muscle and by 31% in human heart sodium channels, while slowing the decay of sodium current in both channel types.
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