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. 2006 Jul 18;103(30):11393–11398. doi: 10.1073/pnas.0603861103

Fig. 4.

Fig. 4.

WIN activates calcineurin in TG neurons and dephosphorylates TRPV1. (A) Calcineurin subunits are coexpressed with TRPV1. The colocalization of calcineurin A subunit (Upper) and B subunit (Lower) with TRPV1 is demonstrated in the respective panels. (B) The effect of various treatments on the nuclear translocation of NFATc4 (calcineurin activation). Cultured TG neurons were exposed to vehicle, ionomycin (1 μM), capsaicin (1 μM), WIN (25 μM), or WIN+CAIP (25 μM/50 μM), and immunohistochemistry was performed by using an antibody against NFATc4. (C) Graphical representation of the percent of NFATc4 positive neurons showing nuclear translocation of NFAFc4 after treatment with VEH/VEH, VEH/WIN (25 μM), CAIP (50 μM)/WIN, VEH/CAP (1 μM), or CAIP (50 μM)/CAP (n = 4 independent cultures assessed by blinded observer; n = 152–180 cells per condition; ∗∗, P < 0.01, ANOVA with Bonferroni post hoc test). (D) Effect of WIN and CAIP/WIN treatment on TRPV1 phosphorylation. Cultured TG neurons (6 ganglia per 10-cm plate) were treated with VEH, WIN (25 μM), or CAIP (50 μM)+WIN. A representative Western blot demonstrating phosphothreonine content (Upper) in TRPV1 immunoprecipitated TG lysates (Lower). (E) Quantification of multiple experiments performed as described in D. The band density was normalized to total TRPV1 protein (n = 3 independent cultures; ∗, P < 0.05, ANOVA with Bonferroni post hoc test).