Figure 6: Δ9-Tetrahydrocannabiorcol activates TRPA1 and causes spinal antinociception. | Nature Communications

Figure 6: Δ9-Tetrahydrocannabiorcol activates TRPA1 and causes spinal antinociception.

From: TRPA1 mediates spinal antinociception induced by acetaminophen and the cannabinoid Δ9-tetrahydrocannabiorcol

Figure 6

(a) Application of Δ9-tetrahydrocannabiorcol (16, filled circles), allyl isothiocyanate (empty circles) and Δ9-tetrahydrocannabinol (filled squares) evoke concentration-dependent [Ca2+]i responses in HEK293 cells expressing human TRPA1 (orange), but not in untransfected cells (black). Data show mean±s.e.m. of three to five experiments, each performed in triplicate. (b) In DRG neurons cultured from Trpa1+/+ mice, 20 μM Δ9-tetrahydrocannabiorcol produced [Ca2+]i responses in 38% of the neurons. In DRG cultures from Trpa1−/− mice, Δ9-tetrahydrocannabiorcol only increased [Ca2+]i in 3% of the neurons. (c) Intrathecal injections of Δ9-tetrahydrocannabiorcol (12 ng in left panel and 120 ng in right panel) significantly and reversibly increased the paw-withdrawal latency in the hot-plate test (53 °C) in Trpa1+/+ mice (empty circles), but were without effect in Trpa1−/− animals (filled circles). Data show mean±s.e.m. for 6 mice per group. *P<0.05; ***P<0.001 compared with pre-injection latency (ANOVA followed by Tukey's HSD test). The scale bar represents 200 μm.

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