In this paper, Peng et al. demonstrate that microglia and monocytes are necessary for the development of neuropathic pain hypersensitivity in the SNT model. Given the recent interest in microglial roles in the pathogenesis of neuropathic pain, this paper makes a very important contribution by providing the first solid demonstration of the necessity of microglia to NP. Moreover, the use of a temporally controlled ablation method allowed the authors to identify a critical window during which microglia drive pain hypersensitivity (early).
There is much to like about this paper, but there are also some methodological concerns. Because of the genetic ablation model that was used, microglia were depleted throughout the CNS, not just the spinal cord. Although they showed that the mice had normal pain sensibility before injury, I wonder whether the depletion of brain microglia did not affect supraspinal processing of pain, complicating the interpretation of spinal microglia’s role.
What do you think?