This study shows that peripheral nerve injury induces a large GluN2A-mediated increase in N-methyl-D-aspartate receptor (NMDAR) activity in spinal lamina II, but not lamina I, neurons. However, NMDAR currents in spinal dorsal horn neurons are not altered in rat models of diabetic neuropathic pain and resiniferatoxin-induced painful neuropathy. Casein kinase II (CK2) inhibitors normalize increased NMDAR currents of dorsal horn neurons in nerve-injured rats. Furthermore, nerve injury significantly increases CK2α and CK2β protein levels in the spinal cord, and inhibition of CK2 or CK2β knockdown at the spinal level substantially reverses pain hypersensitivity induced by nerve injury. These results indicate that neuropathic pain conditions with different etiologies do not share the same mechanisms, and increased spinal NMDAR activity is distinctly associated with traumatic nerve injury.
See article at J Pharmacol Exp Ther 2014, 350:301–312.
- Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics