Fig. 2.

D1DR/D2DR antagonists abolished NMDA-triggered Ca²⁺ up-regulation and inhibited the expression of p-NR1, p-NR2B in the spinal cord, and D1DR/D2DR antagonists induced inhibition of spinal neurons could be reversed by NMDA. (a, b) Representative traces and AUCs of SCH 23,390 (trace 2)/L-741,626 (10 μM) (trace 3), NMDA (trace 4) of the Ca²⁺ oscillations and the effect of SCH 23390/L-741,626 on NMDA (trace 5, 6)-induced upregulation of Ca²⁺ in spinal neurons (n = 3, # P < 0.05, ## P < 0.01, compared with Vehicle group, * P < 0.05, ** P < 0.01, compared with NMDA group, Vehicle: Locke’s buffer). (c, d, e) The expression of p-NR1 and p-NR2B in TCI rats after administration of SCH 23,390 and L-741,626 (n = 4, # P < 0.05, ## P < 0.01, compared with Sham + Vehicle group, *P < 0.05, **P < 0.01, compared with TCI + Vehicle group, p-NR1/NR1 is the expression of (p-NR1/GAPDH)/(NR1/GAPDH), p-NR2B/NR2B is the expression of (p-NR1/GAPDH)/(NR1/GAPDH)). (f, g, h) Immunofluorescence results indicated spinal CGRP and c-Fos expression in TCI rats after SCH 23390/L-741,626 was administrated for 2 h or after the coadministration of NMDA with SCH 23390/L-741,626, respectively (NMDA was administrated 15 min before SCH 23,390 or L-741,626) (n = 4, # P < 0.05, ## P < 0.01, compared with Sham + Vehicle group, * P < 0.05, ** P < 0.01, compared with TCI + Vehicle group, & P < 0.05, && P < 0.01, compared with TCI + SCH 23390/L-741,626 group).