Background It has been reported that mu-opioid receptor activation leads to a sustained
increase in glutamate synaptic effectiveness at the N-methyl-D-aspartate (NMDA) receptor
level, a system associated with central hypersensitivity to pain. One hypothesis is that
postoperative pain may result partly from the activation of NMDA pain facilitatory processes
induced by opiate treatment per se. The authors tested here the effectiveness of the opiate
analgesic fentanyl for eliciting a delayed enhancement in pain sensitivity. Methods The …