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Figure 5 | Molecular Pain

Figure 5

From: Sensitization of TRPV1 by EP1 and IP reveals peripheral nociceptive mechanism of prostaglandins

Figure 5

PGI2 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 (-).

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