Fig. 9. Spinal N -methyl-d-aspartate (NMDA) receptor-mediated ephrinB1-Fc-induced hyperalgesia and increase of expression of phosphorylated mitogen-activated protein kinases (p-MAPKs). NMDA antagonist (+)-5-methyl-10,11-dihydro-SH-dibenzo[a ,d ]cyclohepten-5,10-imine maleate (MK-801) (2.5-μg) was injected at 30 min before intrathecal (i.t.) injection of ephrinB1-Fc (0.5 μg). (A ) Schematic illustration of experimental protocol. (B ) The thermal hyperalgesia tested by paw-withdrawal latency (PWL) and mechanical allodynia tested by paw-withdrawal threshold (PWT) induced by ephrinB1-Fc (0.5 μg) were inhibited by pretreatment with MK-801 (2.5 μg). *P < 0.05 from 0.5 to 4 h, MK-801+ephrinB1-Fc vs. ephrinB1-Fc, n = 8 mice in each group. (C ) The representative immunohistochemical staining and the quantitative data for the decreased ephrinB1-Fc-induced Fos expression by pretreatment with MK-801 (2.5 μg) in the spinal cord of mice. **P < 0.05 compared with ephrinB1-Fc group, n = 6 mice in each group, Scale bar = 100 μm. (D ) The representative bands and the quantitative data for the decreased expression of spinal p-p38, p-ERK, and p-JNK by intrathecal injection of ephrinB1-Fc (0.5 μg) after pretreatment with MK-801. The fold change for the density of each p-MAPKs normalized to total MAPKs for each sample. The fold change of p-MAPKs levels in ephrinB1-Fc group was set at 1 for quantifications. *P < 0.05, compared with ephrinB1-Fc group, n = 4 mice in each group.