Figure 2.
RvE1 inhibits substance P- (SP-) induced potentiation of capsaicin in nociceptive neurons. (a) Capsaicin (CAP, 200 nM) produced consistent [Ca2+]i responses without desensitization after repetitive application (intervals of 8~10 min). Cell viability of neurons was confirmed by their response to high K+ (50 mM KCl solution) at the end of the experiment. n = 18. (b) RvE1 (3 nM) completely inhibited capsaicin-induced [Ca2+]i in capsaicin-responsive neurons. Neurons were perfused with RvE1 (3 nM) for 5 min before the third application of capsaicin. n = 35. (c) Summary of [Ca2+]i responses relative to peak amplitude of first capsaicin responses. Note that RvE1 (1 nM) inhibits 70% of capsaicin-induced [Ca2+]i. Results are presented as the mean ± SEM. ∗ P < 0.05; t-test versus second capsaicin treatment. (d) Substance P (2 μM) enhanced capsaicin- (200 nM) induced [Ca2+]i in small dorsal root ganglion (DRG) neurons (n = 29/40). Neurons were perfused with substance P (2 μM) for 10 min before the second application of capsaicin. (e) RvE1 (1 nM, 5 min) completely inhibited substance P-induced potentiation of capsaicin in small DRG neurons. n = 20 (f) Summary of [Ca2+]i responses relative to peak amplitude of first capsaicin responses. Note that RvE1 (0.5 nM) inhibits 45% of substance P-induced potentiation of capsaicin. Results are presented as the mean ± SEM. ∗ P < 0.05; t-test versus second capsaicin treatment. # P < 0.05; t-test versus first capsaicin treatment.