Figure 6.

Nmb increased neuronal excitability of TG neurons. A-C, exemplary current traces (left panel) and summary data (right panel) show the effects of Nmb (100 nM) on voltage-gated Na⁺ channel (Na_v) currents (A), high-voltage activated (HVA) Ca²⁺ channel currents (B), transient outward A-type K⁺ currents (I_A, upper, C) and the sustained delayed-rectifier K⁺ currents (I_DR, lower, C) in TG neurons, respectively. *p < 0.05 versus control, two-tailed t test. D, representative traces (left panel) and summary data (right panel) indicate that 100 nM Nmb markedly increased the action potential (AP) firing rate (n = 17). **p < 0.01 versus control, two-tailed t test. E, summary data indicate that Nmb at 100 nM had no effect on the resting membrane potential (RMP), but significantly decreased the rheobase of neuronal excitability (n = 17). *p < 0.05 versus control, two-tailed t test. F, summary data show that pretreating TG neurons with KT-5720 (1 μM) abolished the Nmb-induced response in AP firing rate (n = 12). G, representative traces (left panel) and summary data (right panel) show that NiCl₂ (Ni²⁺) at 50 μM completely prevented the Nmb-mediated neuronal hyperexcitability (n = 11). H, left panel, representative traces from a Nmb-sensitive neuron. right panel, summary data indicate that the threshold was +0.98 nA in control and +0.79 nA in neurons treated with 100 nM Nmb. **p < 0.01 versus control, two-tailed t test. I, summary data show Ni²⁺ at 50 μM completely prevented the Nmb-induced lower threshold (n = 9).