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. 2020 Aug 13;28:139–148. doi: 10.1016/j.jare.2020.08.005

Fig. 5.

Fig. 5

D1DR/D2DR activated NMDAR-MAPKs to promote bone cancer pain through Src in a Gαq protein-dependent manner. (a) The mechanical thresholds of TCI rats after administration of Gαq inhibitor YM 254,890 or co-administration of YM 254,890 with NMDA (n = 6, * P < 0.05, ** P < 0.01, compared with 0 h, # P < 0.05, ## P < 0.01, compared with TCI + Gαq inhibitor group, &P < 0.05, &&P < 0.01, compared with Sham + Vehicle group, Vehicle: 2% DMSO) (NMDA was administered 30 min before PP2 treatment). (b) Gαq protein expression in TCI rats after administration of SCH 23390/L-741,626. (c) p-Src expression in TCI rats after administration of Gαq inhibitor YM 254890. (d, e, f) The expression of p-p38, p-ERK, and p-JNK in TCI rats after co-administration of the Gαq inhibitor YM 254,890 with NMDA. (n = 4, # P < 0.05, ## P < 0.01, compared with Sham + Vehicle group, * P < 0.05, ** P < 0.01, compared with TCI group, &P < 0.05, && P < 0.01, compared with TCI + Gαq inhibitor group, p-Src/Src is the expression of (p-Src/GAPDH)/(Src/GAPDH), p-MAPKs/MAPKs is the expression of (p- MAPKs/GAPDH)/(MAPKs/GAPDH)).