Research paperEffects of chronic constriction injury and spared nerve injury, two models of neuropathic pain, on the numbers of neurons and glia in the rostral ventromedial medulla

- We examined whether RVM neurons were lost in two models of neuropathic pain, chronic constriction injury (CCI) and spared nerve injury (SNI).
- Tactile hypersensitivity was observed after both CCI and SNI.
- RVM neuronal loss was not observed ten days after either CCI or SNI.
- RVM neuronal death would be expected to result in glial proliferation (gliosis). Gliosis was not observed 10 days after either CCI or SNI.
- We conclude that loss of RVM neurons is not required for development of hypersensitivity after CCI or SNI.

In previous studies we have reported that spinal nerve ligation (SNL), a model of neuropathic pain, results in the loss of over 20% of neurons in the rostral portion of the ventromedial medulla (RVM) in rats, 10 days after SNL. The RVM is involved in pain modulation and we have proposed that loss of pain inhibition from the RVM, including loss of RVM serotonin neurons, contributes to the increased hypersensitivity observed after SNL. In the present study we examined whether RVM neuronal loss occurs in two other models of neuropathic pain, chronic constriction injury (CCI) and spared nerve injury (SNI). We found no evidence for neuronal loss 10 days after either nerve injury, a time when robust tactile hypersensitivity is present in both CCI and SNI. We conclude that loss of RVM neurons appears not to be required for expression of tactile hypersensitivity in these models of neuropathic pain.