p38 Mitogen-Activated Protein Kinase Is Activated after a Spinal Nerve Ligation in Spinal Cord Microglia and Dorsal Root Ganglion Neurons and Contributes to the Generation of Neuropathic Pain
By Shan-xue Jin, Z. Zhuang, Clifford J. Woolf, R. Ji. Journal of Neuroscience, 2003
839 citations recorded by the source corpus.
Subfields: Neurology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/aab6a82edfff885d7cefb4caf8ccaa42ed48f761
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Neurology
- Clifford J. Woolf
- R. Ji
- Jürgen Sandkühler
- Linda R. Watkins
- M. Suter
- Stephen G. Waxman
- B. Hains
- Yong‐Jing Gao
In Pharmacology
- Clifford J. Woolf
- R. Ji
- Jürgen Sandkühler
- Linda R. Watkins
- M. Suter
- E. Milligan
- Yong‐Jing Gao
- J. Scholz
In Physiology
- Clifford J. Woolf
- R. Ji
- Jürgen Sandkühler
- M. Suter
- Linda R. Watkins
- Yong‐Jing Gao
- E. Milligan
- J. Scholz
Citations in the corpus
- The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, neutral): “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).”
- MAP kinase and pain (2008, background): “Katsura et al. (2006) showed that Src-family kinases are also activated in spinal microglia after SNL and contribute to the activation of ERK but not p38 in spinal microglia.”
- Glia and pain: Is chronic pain a gliopathy? (2013, background): “IBA1 is probably the most widely used marker for microglial reaction in the pain field, partly because the IBA1 antibody from Wako Chemicals works better than other antibodies of microglial markers.”
- The neuropathic pain triad: neurons, immune cells and glia (2007, background): “Nerve injury-induced microglial activation is characterized by phosphorylation (activation) of p38 MAP kinase, extracellular signal-related kinase (ERK) isoforms 1 and 2, and the Src-family kinases (Src, Lck and Lyn”
- Central sensitization and LTP: do pain and memory share similar mechanisms? (2003, background): “Activated microglia in the dorsal horn seem to have a particular role in inducing neuropathic pain [85], including one that involves p38 MAPK [ 86 ,87].”
- Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury (2006, background): “nerve ligation (Jin et al., 2003), and sciatic nerve inflammation”
- p38 MAPK, microglial signaling, and neuropathic pain (2007, methodology): “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].”
- Role of the Immune system in chronic pain (2005, background): “The recruitment of microglia is commonly associated with the activation (phosphorylation) of p38 MAP kinas”
- Distinct roles of matrix metalloproteases in the early- and late-phase development of neuropathic pain (2008, background): “Because we have previously shown that SNL activates p38 mitogen-activated protein kinase (MAPK) in spinal microgli”
- Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, background): “vivo (Jin et al., 2003; Kim et al., 2002; Svensson et al., 2003; Tsuda et al., 2004), and is suggested to play a role in the early induction of neuropathic and inflammatory pain.”
- ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model (2005, methodology): “The specificity of the staining and antibodies has been tested in previous studies (Ji et al., 1999, 2002a; Jin et al., 2003), and immunofluorescence results were confirmed with diaminobenzidine (DAB) staining using the ABC method (Ji et al., 1994).”