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. Author manuscript; available in PMC: 2009 Sep 15.
Published in final edited form as: Pain. 2008 Apr 1;138(3):604–616. doi: 10.1016/j.pain.2008.02.022

Figure 7. AKAP150/PKA association is necessary for TRPV1 phosphorylation and sensitization.

Figure 7

A.) Cultured TG neurons pre-treated with tris/H20 veh, St-HT31P (50 μmol), or StHT31P-C (50 μmol) 15 min, followed by 8-Br-cAMP (10 mM, 5 min), and analyzed for TRPV1 phosphorylation by autoradiographic densitometry normalized to Western blot immunoreactivity. *p<0.05, NS = not significant.

B.) Rats were injected with 50 μl Tris/saline veh, St-HT31P (5 μmol), or St-HT31P-C (5 μmol) in the right hindpaw. The same paws were injected with 0.01% ethanol/saline veh or 0.3 μg PGE2 15 min later, upon which thermal paw withdrawal latencies were measured by blinded observers. Data are depicted as change in paw withdrawal latency (sec) from baseline valuations taken before injections, such that PGE2 produces shorter paw withdrawal latency values vs. baseline). All plotted data expressed as mean ± SEM, n= 6–10 animals per group, two-way ANOVA with Bonferroni post hoc test, **p<0.01, NS=not significant.