Fig. 2.  QX-314 activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) channels expressed in Xenopus laevis  oocytes. (A ) QX-314 (chloride; 10–60 mM) produced inward currents in a concentration-dependent manner in an oocyte expressing TRPV1 channels. Each concentration was applied for 10 s with a 2-min washout period; the holding potential was −60 mV. For comparison and as a positive control, each experiment was flanked by capsaicin application at a concentration producing a near-maximal response (50 μM). The organic cation, N -methyl-d-glucamine chloride (60 mM), applied as a negative control, produced negligible activation. (B ) Traces from a similar experiment performed with lidocaine. Lidocaine (10–60 mM) produced TRPV1-mediated inward currents in a concentration-dependent manner, whereas N -methyl-d-glucamine (60 mM) was without significant effect. (C ) Mean peak current amplitudes ± SEM of experiments described in A  and B , normalized to responses produced by 50 μM capsaicin (I  norm). QX-314 produced 0.4 ± 0.1% (10 mM), 3.5 ± 1.3% (30 mM), and 21.5 ± 6.9% (60 mM) of the maximal capsaicin-evoked current (n = 12); lidocaine produced 2.5 ± 0.4% (10 mM), 8.8 ± 2.0% (30 mM), and 21.1 ± 5.0% (60 mM) of the maximal capsaicin-evoked current (n = 6). N -methyl-d-glucamine produced 0.6 ± 0.4% of the responses evoked by 60 mM QX-314 (n = 9). ***P < 0.001. NMDG =N -methyl-d-glucamine.

Fig. 2.  QX-314 activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) channels expressed in Xenopus laevis  oocytes. (A ) QX-314 (chloride; 10–60 mM) produced inward currents in a concentration-dependent manner in an oocyte expressing TRPV1 channels. Each concentration was applied for 10 s with a 2-min washout period; the holding potential was −60 mV. For comparison and as a positive control, each experiment was flanked by capsaicin application at a concentration producing a near-maximal response (50 μM). The organic cation, N -methyl-d-glucamine chloride (60 mM), applied as a negative control, produced negligible activation. (B ) Traces from a similar experiment performed with lidocaine. Lidocaine (10–60 mM) produced TRPV1-mediated inward currents in a concentration-dependent manner, whereas N -methyl-d-glucamine (60 mM) was without significant effect. (C ) Mean peak current amplitudes ± SEM of experiments described in A  and B , normalized to responses produced by 50 μM capsaicin (I  norm). QX-314 produced 0.4 ± 0.1% (10 mM), 3.5 ± 1.3% (30 mM), and 21.5 ± 6.9% (60 mM) of the maximal capsaicin-evoked current (n = 12); lidocaine produced 2.5 ± 0.4% (10 mM), 8.8 ± 2.0% (30 mM), and 21.1 ± 5.0% (60 mM) of the maximal capsaicin-evoked current (n = 6). N -methyl-d-glucamine produced 0.6 ± 0.4% of the responses evoked by 60 mM QX-314 (n = 9). ***P < 0.001. NMDG =N -methyl-d-glucamine.

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