We recently showed that the increase in nNOS activity in the superficial dorsal horn of the spinal cord reflects a neuropathic pain state even 1 week after nerve injury [20] and that this nNOS activation may be reversibly regulated by the translocation of nNOS from the cytosol to the plasma membrane in the presence of NMDA and the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) [21]. This evidence concerns the gene NOS1 and injury.