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Fig. 1 | Molecular Pain

Fig. 1

From: Anoctamin-1 Cl channels in nociception: activation by an N-aroylaminothiazole and capsaicin and inhibition by T16A[inh]-A01

Fig. 1

ANO1 currents are induced by ANO1-activator and diminished by ANO1-inhibitor in mouse DRG neurons and transfected HEK-293 cells. a Traces of currents recorded to voltages ramped from −100 to +100 mV of a representative mANO1 transfected HEK-293t cell (mANO1-HEK293): before perfusion (blue trace Pre) and following bath perfusions of N-aroylaminothiazole (E-act, 10 µM, red trace) activating ANO1, and sequential inhibition of E-act effects by mixing in ANO1-inhibitor T16A[inh]-A01 (ANO1-inh, 20 µM, green trace). Recording pipettes had 0-Ca2+; VH = 0 mV. b Averaged current sizes recorded at −80 mV and +80 mV (black lines), increased following 10 µM E-act (black bar at 70 s) and decreased by ANO1-inh with E-act (white bar at 140 s) bath perfusions for mANO1-HEK293 cells (n = 3). Gray lines represent SE. c Traces of ANO1-like outwardly rectifying currents recorded to voltages ramped from −100 to +100 mV of a representative DRG neuron: before activation (blue trace Pre), activation by 10 µM E-act (red trace) bath perfusion, and inhibition by a perfusion mixture of E-act with 20 µM ANO1-inh (green trace). d Average current sizes recorded at −80 mV and +80 mV (black lines), following 10 µM E-act (black bar at 80 s) perfusion and a sequential perfusion mixture of 20 µM ANO1-inh with E-act (white bar at 180 s) for DRG neurons (n = 7). Gray lines represent SE. In DRG neurons (c, d), all bath and applications contained 10 µM ruthenium red to block TRP channels and recording pipette contained 0-Ca2+. VH = −70 mV. All intracellular solutions were CsCl-based. Records of currents were made over 200 ms at 1 Hz intervals in the whole-cell configuration

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