Figure 5From: Sensitization of TRPV1 by EP1 and IP reveals peripheral nociceptive mechanism of prostaglandinsPGI2 causes potentiation or sensitization of TRPV1 through mainly through PKC activation. (A) Representative traces of potentiation of capsaicin-activated currents by PGI2 (1000 nM, 1.5 min), a specific IP agonist, ONO-54918-07 (1.5 min) or PGI2 (100 nM, 6.5 min), but not by PGI2 (100 nM, 1.5 min) in mouse DRG neurons. Vh: -60 mV. (B) Effects of treatments (1.5 or 6.5 min) with PGI2 (100 or 1000 nM), ONO-54918-07 (IP Agon., 100 nM), PGI2 (1000 nM) plus ONO-8713 (EP1 Antg., 1 μM), PGI2 (1000 nM) plus U73122 (3 μM), PGI2 (1000 nM) plus U73343 (3 μM) or PGI2 (1000 nM) plus PKCε-I (200 μM) on capsaicin-activated currents in DRG neurons from wild type (IP+/+) mice, and effects of PGI2 on capsaicin-activated currents in DRG neurons from IP-deficient (IP-/-) mice. Currents are normalized as described in Figure 1. * p < 0.05 vs. Cont. ++ p < 0.01 vs. U73343, # p < 0.05, ## p < 0.01 vs. PGI2 (1000 nM, 1.5 min) in DRG neurons from IP+/+ mice. Numbers in parenthesis indicate cells tested. (C) A representative trace of potentiation of capsaicin-activated currents by PGI2 (1000 nM, 1.5 min) in HEK293 cells expressing both TRPV1 and IP. Vh: -60 mV. (D) Effects of treatments (1.5 or 6.5 min) with PGI2 (100 or 1000 nM) or PGI2 (1000 nM) plus calphostin C (Calp. C, 1 μM) on capsaicin-activated currents in HEK293 cells expressing rat wild type TRPV1 or S502A/S800A mutant with IP. Currents are normalized as described in Figure 1. * p < 0.05 vs. Cont. (E) Temperature threshold for TRPV1 activation in the presence of PGI2 (32.2 ± 1.2°C) was significantly lower than that in the absence of PGI2 (38.2 ± 0.5°C) in HEK293 cells expressing rat TRPV1 and IP. * p < 0.01 vs. PGI2 (-).Back to article page