Skip to main content
Figure 2 | Molecular Pain

Figure 2

From: PKCε-dependent potentiation of TTX-resistant Nav1.8 current by neurokinin-1 receptor activation in rat dorsal root ganglion neurons

Figure 2

Effect of NK-1 agonist Sar-SP on Na v 1.8 currents. A: time course of the potentiation effect of Sar-SP. The maximal increase in the peak amplitude was at 3 min after Sar-SP perfusion, and reduced slowly to control level thereafter. B: typical traces illustrating the Nav1.8 current recorded in a neuron pre- (dashed line, control) and post- (solid line, Sar-SP) perfusion of 1 μM Sar-SP. C: histogram showing the effect of 1 μM and 10 μM Sar-SP. The normalized peak current was enhanced to 116.2 ± 2.9% and 117.1 ± 1.4% 3 min after perfusion of 1 μM and 10 μM Sar-SP, respectively (***p < 0.001, versus control, Kruskal-Wallis one-way ANOVA, n = 16 for control, 13 for 1 μM, and 6 for 10 μM). D: NK-1 antagonist Win51708 (5 μM) completely blocked the effect of Sar-SP in all 15 neurons tested (p > 0.05, t-test). E: The rate of the Sar-SP-responsive cells was increased after CFA-treatment. F: The effect of Sar-SP was also increased after peripheral CFA-treatment (* p < 0.05, t-test, n = 8 for saline and 14 for CFA-treated). G and H: Sar-SP shifted the activation (G) and steady-state inactivation (H) curve in a hyperpolarizing direction.

Back to article page