GLIA: A novel drug discovery target for clinical pain
By Linda R. Watkins, S. Maier. Nature reviews. Drug discovery, 2003
687 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/aa129c1592a620cfee48124cc2953beab3bdfa81
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In Cellular and Molecular Neuroscience
In Pharmacology
In Physiology
Citations in the corpus
- Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, background): “However, it is now clear that spinal cord glial cells (microglia and astroglia) importantly contribute to pain facilitation (reviewed in DeLeo and Yezierski, 2001; Watkins and Maier, 2003; Watkins et al., 2001).”
- Pathological and protective roles of glia in chronic pain (2009, background): “Targeting glia for pain control Therapeutic strategies to control neuropathic pain states by targeting glial functio”
- 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): “When microglia and astrocytes are activated in the spinal cord under pathological pain conditions, they synthesize multiple inflammatory mediators, and may activate each other (DeLeo and Yezierski, 2001; Watkins and Maier, 2003; Watkins et al., 2001).”
- p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “Several p38 MAPK inhibitors including SB281838, BIRB0796, Ro320-1195, and SCIO469 have been tested in clinical trials for inflammatory diseases such as rheumatoid arthritis as well as for cancer [67,68].”
- The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “Astrocyte activation is morphologically characterised by hypertrophy and increased production of intermediate filaments, glial fibrillary acidic protein (GFAP), vimentin and/or nestin, and functionally by increased production of a variety of pro-inflammatory substances (Watkins and Maier, 2003).”