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. 2012 Jun 4;209(6):1121–1134. doi: 10.1084/jem.20120242

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© 2012 Xiong et al.

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Figure 4. — DH-CBD rescue of PGE₂-induced inhibition of the α3 GlyRs and chronic pain. (A) Trace records of I_Gly in HEK 293 cells coexpressing EP2 receptors with either the α3 or α1 GlyRs before and after sustained PGE₂ application. (B) Time courses of I_Gly in the cells coexpressing EP2 receptors with either the α3 (n = 6) or α1 (n = 5) GlyRs after sustained PGE₂ application. ***, P < 0.001 (α1 vs. α3). (C) Trace records of I_Gly in cells coexpressing EP2 receptors with the α3 GlyRs without and with DH-CBD after sustained PGE₂ application. (D) Time courses of DH-CBD potentiation of I_Gly in cells coexpressing the α3 GlyRs and EP2Rs after sustained PGE₂ application (n = 6). ***, P < 0.001 as compared with vehicle application. (E) Time courses of PWL to thermal stimulation before, during, and after i.t. PGE₂ injection in WT and α3^−/− mice (n = 10). ***, P < 0.001, as compared with the WT mice. (F) The analgesic effect of 50 mg/kg DH-CBD i.p. (n = 10) on PWL to thermal stimulation after i.t. PGE₂ injection. *, P < 0.05; ***, P < 0.001, as compared with i.p. vehicle (n = 10). Data are representative of two independent experiments and expressed as mean ± SEM.