Coupling of serotonergic input to NMDA receptor-phosphorylation following peripheral nerve injury via rapid, synaptic up-regulation of ND2

C fiber-evoked dorsal horn field potentials were increased 60 min after SNL by superfusion with NMDA agonist cis-ACPD at 100 nM (p < 0.01 at the Bonferroni test), however cis-ACPD was effective only at 10 μM following prior administration of rotenone. Rotenone also abolished enhancement of evoked potentials induced by simultaneous stimulation of NMDA and 5-HR2B receptors in uninjured rats. Increased postsynaptic up-regulation of ND2/pNMDAR 60 min after SNL was prevented by prior administration of selective 5-HT2B antagonist SB204741. These results support a pivotal role for ND2 in coupling serotonergic input to NMDAR-activation during neuropathic pain.