Voltage-gated sodium channels (Na_V) are pres­ent in most excitable cell membranes and play an important role in generating action potentials. A variety of toxins and chemi­cals are known to either block or modu­late Na⁺ channels and have proven to be invaluable in investigating the physiological characteristics of these channels¹. Most notably, tetrodotoxin (TTX), a potent and selective blocker of Na⁺ channels, binds to neurotoxin receptor site 1 to block them².

Aconitine is a diterpense two-ester alkaloid derived from the tubers of aconitinum plants and has been used as traditional herbal medicine in China and Japan since ancient times. Modern pharmacological studies have shown that aconitine has effects of analgesia and anesthesia, anti-inflammatory, immune regulation, anti-tumor and cardiotonic actions^3,4. Concurrently, aconitine also presents enormous toxicity⁵. It is well known for its toxic effects on the heart and central nervous system where it causes cardiac arrhythmias, systemic paralysis and coma⁶. Aconitine alters the kinetics and voltage dependence of Na⁺ chan­nel activation, inhibits Na⁺ channel inactivation through binding to neurotoxin receptor site 2 and causes persistent activation of Na⁺ channels at the resting mem­brane potential⁷.