Fig. 6. NMDA-mediated synaptic transmission during physiological state (A) and nerve injury state (B).

Binding of glutamate and co-agonist D-serine to NMDA receptor subunit modulates synaptic transmission and plasticity in normal state. Increase in DAAO activity after nerve injury decreases the levels of D-serine, which may indirectly increase the synthesis of reactive oxygen species to induce neuropathic pain through increased NMDA phosphorylation and consequent enhanced synaptic plasticity.