Neuropathic pain

Abstract

It is now widely appreciated that microglia are critical effectors in the development of persistent pain hypersensitivity after traumatic nerve injury. Data to support this view began to emerge in the 1990s, and presently the neuropathic pain literature is replete with research articles describing various roles of microglia in the pathogenesis of pain. With this rapid proliferation of publications, it may be challenging to distill whether there exists a precise microglial function or phenotype that drives pain hypersensitivity. Numerous signaling pathways and countless molecules have been potentially implicated; however, their point(s) of convergence or divergence in injury-induced aberrant nociceptive processing are unclear. In this chapter, we examine key proposed mechanisms of microglial involvement in pain hypersensitivity. We also interrogate the concept of an inflammatory microglia phenotype and peripheral immune cell trafficking to spinal cord dorsal horn induced by nerve injury.