Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats
By E. Milligan, C. Twining, M. Chacur, J. Biedenkapp, Kevin A. O’Connor, S. Poole, Kevin J. Tracey, David A. Martin, S. Maier, Linda R. Watkins. Journal of Neuroscience, 2003
680 citations recorded by the source corpus.
Subfields: Anesthesiology and Pain Medicine, Physiology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/7544ede4d5c8d657109fc78ec8187b15e208ded0
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Citations in the corpus
- Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, methodology): “Thereafter, rats received 4 mg perisciatic zymosan every other day to maintain persistent SIN as previously described (Milligan et al., 2003).”
- p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “However, further studies suggest that inhibition of p38 is also able to reverse neuropathic pain symptoms in different animal models [34,38,40,44,46].”
- MAP kinase and pain (2008, background): “Moreover, intrathecal infusion of p38 inhibitors attenuates neuropathic pain in different animal models (Jin et al., 2003; Milligan et al., 2003; Schafers et al., 2003; Tsuda et al., 2004; Hains and Waxman, 2006).”
- Cytokines, Inflammation, and Pain (2007, background): “It has been well demonstrated that spinal glial activation is necessary for induction of the neuropathic pain state [30,41,42].”
- Inhibition of Microglial Activation Attenuates the Development but Not Existing Hypersensitivity in a Rat Model of Neuropathy (2003, background): “These procedures include spinal nerve injury (Sweitzer et al., 2001; Raghavendra et al., 2002), peripheral inflammation (Watkins et al., 1997; Bao et al., 2001), peripheral nerve inflammation (Milligan et al., 2003), and chronic opioid treatment (Raghavendra et al., 2002).”
- Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α (2005, background): “Similarly, the effects of TNF could contribute to the modification of circuit behavior that underlies the hyperalgesia after peripheral nerve damage, a neuropathological state that involves glia-released cytokines, including TNF (Watkins et al., 2001; Milligan et al., 2003).”
- The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, neutral): “…image pain involving the contralateral spread of pain, was reversed by intrathecal administration of fluorocitrate, a glial metabolic inhibitor (Milligan et al., 2003) possibly due to decoupling of spinal gap junctions which prevents activation of distant glia and release of…”
- Glia and pain: Is chronic pain a gliopathy? (2013, background): “Interestingly, even acute opioid treatment after a subcutaneous injection results in marked SGC reaction in DRGs at 2 hours when morphine analgesia declines [18] (Table 1).”
- Models and mechanisms of hyperalgesia and allodynia. (2009, background): “An early report has shown that peripheral inflammation of a hindpaw by intraplantar zymosan injections leads to mechanical and thermal hyperalgesia which involves spinal glia: selective inhibition of glial metabolism by intrathecal administration of fluorocitrate results in a marked, but reversible,”
- Neural plasticity after peripheral nerve injury and regeneration. (2007, background): “In addition, spinal glial cells release proinflammatory cytokines and excitatory neuromodulators after axonal injuries, which once central sensitization is initiated, enhance the hyperexcitability of dorsal horn neurons (Watkins et al., 2001; Milligan et al., 2003; Ohtori et al., 2004).”