Inhibition of Microglial Activation Attenuates the Development but Not Existing Hypersensitivity in a Rat Model of Neuropathy

By V. Raghavendra, F. Tanga, J. Deleo. Journal of Pharmacology and Experimental Therapeutics, 2003

797 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/0a0018020cb0f8636f7f0b5bed660a4b420166cf

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Citations in the corpus

ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model (2005, background): “A microglial inhibitor, minocycline, reduces neuropathic pain (Raghavendra et al., 2003), possibly by suppressing p38 activation (Tikka et al.”
Minocycline: far beyond an antibiotic (2013, background): “…minocycline can exert anti-nociceptive effects on experimental neuropathic pain induced by peripheral nerve injury, inflammation or SCI, after both systemic (i.p.) and local (intrathecal) administration (Raghavendra et al., 2003; Hains and Waxman, 2006; Owolabi and Saab, 2006; Mika et al., 2007).”
Models and mechanisms of hyperalgesia and allodynia. (2009, neutral): “Spinal cord cells consist of the following: 4) spinal dorsal horn neurons that express the neurokinin I receptor (318, 383, 542, 545, 575, 611), 5) microglia (192, 276, 375, 423, 502, 564, 618), and 6) astrocytes (213, 387, 624).”
The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “Indeed following SNL, IL-6 released in the spinal cord leads to STAT3 phosphorylation in microglia, which when blocked, with a JAK2 inhibitor, attenuates pain hypersensitivity (Dominguez et al., 2008).”
Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, background): “These findings are consistent with the effectiveness of minocyline in preventing, but not reversing peripheral nerve injury-induced chronic allodynia and hyperalgesia (Raghavendra et al., 2003), presumably related to inhibition of both microglial and consequent astroglial activation by preemptive mi”
Glia and pain: Is chronic pain a gliopathy? (2013, background): “Of interest, PP2 suppressed the activation of ERK but not p38 in spinal microglia [126].”
Distinct roles of matrix metalloproteases in the early- and late-phase development of neuropathic pain (2008, background): “To define the mechanism by which MMP-9 induces neuropathic pain, we examined microglial activation in the spinal cord, an event essential for the pathogenesis of neuropathic pai”
p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “Similarly, a microglial inhibitor minocycline was shown to prevent/delay neuropathic pain, but not to reverse established neuropathic pain [29,30].”
Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury (2006, background): “…has been shown to inhibit inflammatory cytokines, free radicals production, and matrix metalloproteinases (Stirling et al., 2005) and potently downregulates the activity of microglia in vivo (Raghavendra et al., 2003; Hua et al., 2005; Ledeboer et al., 2005 ), followed by 10 ␮l of aCSF flush.”