Changes in post-tetanic potentiation of A-fiber dorsal horn field potentials parallel the development and disappearance of neuropathic pain after sciatic nerve ligation in rats.

Significant plastic changes in spinal nociceptive processing appear to accompany peripheral nerve injury or inflammation. Using a well-established model of neuropathic pain, we have recently reported that loose ligation of the sciatic nerve was accompanied by a long-lasting post-tetanic potentiation of sciatic-evoked A-fiber superficial dorsal horn field potentials. In the present study we demonstrate that the typical disappearance of thermal hyperalgesia as a behavioral sign of neuropathic pain several weeks after loose sciatic nerve ligation is accompanied by the loss of the long-lasting potentiation. These data suggest that a significant but reversible shift in the processing of sensory information in the spinal dorsal horn follows peripheral nerve injury, and lend further support to the notion that long-lasting synaptic plasticity may contribute to the development of neuropathic pain.