Effect of L-bupivacaine (50 μM) and D-bupivacaine (50 μM) on sodium currents in dorsal root ganglion neurons. (A) A typical trace of tetrodotoxin-sensitive sodium current. Short-lasting currents were completely blocked by 0.2 μM tetrodotoxin, which indicates that these currents are generated as a result of the activation of tetrodotoxin-sensitive sodium channels. (B) A typical trace of tetrodotoxin-resistant sodium current. Long-lasting currents were only partly blocked by 0.2 μM tetrodotoxin, which indicates that these currents are generated as a result of activation of a mixture of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels. (C) Histogram of the distribution of the diameters of dorsal root ganglion neurons that generated tetrodotoxin-sensitive (shaded columns) and tetrodotoxin-resistant (open columns) sodium currents. (D) L-bupivacaine slightly decreased the amplitude of tetrodotoxin-sensitive sodium currents. However, D-bupivacaine dramatically decreased the amplitude of tetrodotoxin-sensitive sodium currents. (E) L-bupivacaine and D-bupivacaine mostly decreased the amplitude of tetrodotoxin-resistant sodium currents. (F) Summary of the blocking effects of L-bupivacaine and D-bupivacaine on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents. L-bupivacaine selectively abolishes the tetrodotoxin-resistant sodium channels without affecting the tetrodotoxin-sensitive sodium channels compared to D-bupivacaine (***P < 0.001). Data presented as mean ± SD.