It is known that painful tissue injury evokes an increase in
dynorphin in spinal neurons. It is not known, however, whether dynorphinergic systems respond similarly to the
pain that accompanies
peripheral neuropathy. Radioimmunoassays and immunocytochemistry were used to evaluate changes in
dynorphin A(1-8) in the spinal cord of rats with a painful
peripheral neuropathy. The neuropathy is the result of a constriction injury that is created by tying loose
ligatures around the common sciatic nerve. Signs of abnormal
pain sensations,
hyperalgesia,
allodynia (
pain after normally innocuous stimuli), and spontaneous
pain (or
dysesthesia), are first detected 2-5 days after injury, reach peak severity in about 10 days, and persist for 2-3 months (Bennett, G. J.; Xie, Y.-K.
Pain 33:87-107; 1988).
Dynorphin increased by 5 days in cells in laminae I-II and V-VII in the lumbar spinal cord ipsilateral to the injury. This increase, maximal
at 10 days (262%), was still present 20 days after the injury but was now seen only in neurons in the deep laminae (V-VII). Thus, the spinal dynorphinergic system appears to respond to
neuropathic pain. Furthermore, our results suggest that dynorphinergic cells in the superficial and deep laminae may have different roles in nociception.