Fig. 4.

Biophysical and pharmacological characterisation of X. tropicalis Tmem16a. (a) Example currents evoked by single depolarizing pulses from − 70 to + 70 mV when [Ca²⁺]_i is 0, 180 (Ca²⁺ EC₂₀) or 338 nM (Ca²⁺ EC₁₀₀), with inhibition in the presence of 10 μm Ani9 shown in green. (b) X. tropicalis Tmem16a conductance is dependent on intracellular calcium levels (black) and inhibited in the presence of Ani9 (green). (c) In whole-cell current-voltage (I-V) tests recorded at 0, 180 & 338 nM [Ca²⁺]_i, the inhibitory effect of Ani9 on maximally-active current (at 338 nM [Ca²⁺]_i) across the voltage range is shown in green. (d–f) Further exploration of X. tropicalis Tmem16a sensitivity to Ani9, conducted at 338 nM (EC₁₀₀) intracellular [Ca²⁺], finds concentration-dependent current inhibition recorded from a single cell at + 70 mV (d). Increasing concentration of Ani9 elicits dose-dependent inhibition of X. tropicalis Tmem16a (e). Both outward and inward chloride movement (recorded at -70 mV and + 70 mV respectively) is sensitive to inhibition by Ani9 (f). (g) X. tropicalis Tmem16a currents are sensitive to a range of frequently-used inhibitor compounds. All compounds were tested on maximally-active X. tropicalis Tmem16a currents (EC₁₀₀ [Ca²⁺]_i, + 70 mV).