Figure 4.
Pharmacological properties of the chimeras. Current records obtained at 100 mV. Temperature, 25°C. A, PIP2 (10 μm) activates the VRctCR channel. B, PIP2 (10 μm) inhibits the CRctVR channel. C, Bar plot of several experiments exposing the CRctVR and VRctCR channels to PIP2 (10 μm). Unpaired t test showed that both chimeras were affected by PIP2 addition. D, Current traces showing menthol-induced activation and La3+ blocking of CRctVR chimera. F, Current traces for capsaicin-induced activation and La3+ blocking of VRctCR chimera. E, G, A summary of the experiments performed for the indicated chimera. La3+ was added to check whether the chimeras were able to be blocked (the addition was always performed after a maximal activation of the respective channel). Capsaicin (Cap) (200 μm) and menthol (Men) (500 μm) were added to CRctVR and VRctCR, respectively, as control experiments. One-way ANOVA and Bonferroni’s statistical analysis were performed for the two data sets in E and G, and in both cases the populations were found to be statistically different (p < 0.05). H, Capsaicin dose–response curves for TRPV1 (IC50, 0.6 μm) and VRctCR (IC50, 7.8 μm). I, Menthol dose–response curves for TRPM8 (IC50, 22 μm) and CRctVR (IC50, 28 μm). Current values were normalized and expressed as percentage of maximal response to the agonist. Each point represents mean values ± SD from at least three different patches. The Hill equation was used to fit the data.