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Fig. 2 | Molecular Pain

Fig. 2

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

Fig. 2

ANO1-activator evokes action potentials in DRG neurons that are dependent on intracellular Cl. a Membrane potential (Vm) trace (black trace) adjusted by current injections (red trace) of a representative DRG neuron are shown to illustrate the protocol of whole-cell current-clamp recordings. The current injections necessary to lower Vm near to −70 mV varied; therefore, they were determined empirically at the start of current clamp. b Average number of action potentials (APs) by DRG neurons over 25 s were significantly increased by ANO1 activation from an N-aroylaminothiazole (E-act, 10 µM, black bars) perfusion compared to prior to application (Pre white bars); when intracellular solution concentrations were 160 mM Cl (high [Cl]i, n = 3) or 40 mM Cl (mid [Cl]i, n = 3), but not 10 mM Cl (low [Cl]i, n = 3). Error bars are SE. (***p > 0.001; **p > 0.01). c APs recorded in representative DRG neurons before application (black Pre) and following perfusion of E-act (red) with intracellular solutions of High [Cl]i (upper graph), Mid [Cl]i (middle graph) or Low [Cl]i (bottom graph). d A representative DRG neuron voltage–time plot of: AP spontaneously occurring before application (broken line), and AP induced by E-act (solid line). (Insert box) APs superimposed upon each other to demonstrate that there was no difference in the shape of the voltage–time plots, only the time of action potential onset

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