The spared nerve injury (SNI) model of peripheral neuropathy produces a robust and long-lasting hypersensitivity. Previous
behavioural studies suggest that brainstem–spinal pathways originating in or relaying through the rostroventromedial medulla (RVM)
contribute to neuropathic hypersensitivity. We determined whether SNI induces changes in response properties of RVM neurons that
might influence descending modulation of nociception. RVM neurons included in the study were classified into presumably
pronociceptive ON-cells and antinociceptive OFF-cells (giving excitatory or inhibitory responses to noxious stimulation, respectively).
Spontaneous activity and the response to cold, pinch and colorectal distension were assessed under light anaesthesia in the rat,
1 week and 8 weeks following nerve injury or sham operation. Spontaneous activity was increased 1 week but not 8 weeks after
nerve injury in ON-cells but decreased in OFF-cells at both time points. In the SNI group, cold-evoked responses were enhanced
particularly in ON-cells, independent of the postoperative time point. Responses of ON-cells to pinch and visceral stimulation were
enhanced 8 weeks but not 1 week following nerve injury, whereas OFF-cell responses to pinch or colorectal distension were not
changed. The results indicate that SNI induces pronociceptive changes in spontaneous activities of ON-cells and OFF-cells and peripherally evoked responses of ON-cells that vary with the postoperative time point. Increased ON-cell activity and decreased OFF-cell activity in the RVM are likely to enhance spinal nociception in a tonic fashion, whereas increased responses of ON-cells to peripheral stimulation are likely to enhance ascending nociceptive signals by a positive feedback following peripheral
noxious stimulation