Erin D. Milligan

TL;DR: The current understanding of the contribution of glia to pathological pain and neuroprotection is reviewed, and how the protective, anti-inflammatory actions ofglia are being harnessed to develop new drug targets for neuropathic pain control is reviewed.

TL;DR: Taken together, these findings suggest a new, dramatically different approach to pain control, as all clinical therapies are focused exclusively on altering neuronal, rather than glial, function.

TL;DR: The present studies demonstrate that both ipsilateral and mirror-image SIN-induced allodynias are reversed by intrathecal (peri-spinal) delivery of fluorocitrate, a glial metabolic inhibitor, and provide the first evidence that ipsilaterally and Mirror-image inflammatory neuropathy pain are created both acutely and chronically through glial and proinflammatory cytokine actions.

TL;DR: In this article, the authors reported that minocycline, a selective inhibitor of microglial cell activation, inhibits low threshold mechanical allodynia, as measured by the von Frey test, in two models of pain facilitation.

TL;DR: Results suggest that IL-1 and fractalkine are endogenous regulators of morphine analgesia and are involved in the increases in pain sensitivity that occur after chronic opiates.