Skip to main content
. 2008 Feb 25;153(7):1538–1549. doi: 10.1038/bjp.2008.33

Figure 6.

Figure 6

PGE2-G-induced thermal hyperalgesia is partially mediated by prostanoid receptors. (a) After determination of baseline withdrawal latencies from a radiant heat source, PGE2 (0.1 μg 50 μl−1, i.pl.) or PGE2 (0.1 μg 50 μl−1, i.pl.) combined with a cocktail of EP1, EP2, EP3 and EP4 antagonists (L-335677, AH6809, L-826266 and L-161982) (20 nmol 50 μl−1, i.pl.) was administered and withdrawal latencies were recorded for the following 160 min. PGE2 (0.1 μg) caused a decrease in withdrawal latency (P<0.0001), which was completely blocked by a cocktail of EP1, EP2, EP3 and EP4 antagonists. (b) Using the same treatment protocol as in (a), PGE2-G (1 μg 50 μl−1, i.pl.) caused a decrease in withdrawal latency, but the cocktail of prostanoid receptor antagonists (20 nmol 50 μl−1, i.pl.) only partially blocked its effects. The degree of reversal was significantly less than that produced by PGE2 (P<0.0001). EP, PGE2 receptor; i.pl., intraplantar; PGE2-G, prostaglandin E2 glycerol ester.