Neuropathic pain and spinal microglia: a big problem from molecules in "small" glia.

By M. Tsuda, Kazuhide Inoue, Michael W. Salter. Trends in Neurosciences, 2005

797 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/0342886a4111652004f2b242edbd1f02bad6246e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. R. Ji
2. M. Suter
3. E. Milligan
4. Linda R. Watkins
5. R. Meyer
6. J. Campbell
7. Jürgen Sandkühler
8. Xavier Navarro

In Neurology

1. R. Ji
2. Jürgen Sandkühler
3. Linda R. Watkins
4. T. Berta
5. M. Suter
6. Maiken Nedergaard
7. E. Milligan
8. G. Burnstock

In Physiology

1. R. Ji
2. Jürgen Sandkühler
3. M. Suter
4. Linda R. Watkins
5. E. Milligan
6. T. Berta
7. Maiken Nedergaard
8. R. Meyer

Citations in the corpus

• Pathophysiology and Therapeutic Potential of Purinergic Signaling (2006, background): “P2X 4 receptors are induced in spinal microglia that appear to gate tactile allodynia after nerve injury (Tsuda et al., 2003, 2005; Inoue et al., 2004, 2005).”
• Mechanisms of neuropathic pain. (2006, background): “In contrast, allodynia is prominent in traumatic neuropathy and cooling often causes severe pain.”
• Neural plasticity after peripheral nerve injury and regeneration. (2007, background): “Activated microglia has also recently been implicated in the development of neuropathic pain, particularly by means of their expression of purinergic receptor P2X4, and of p38 MAPK (Jin et al., 2003; Tsuda et al., 2005).”
• Pathological and protective roles of glia in chronic pain (2009, background): “As described above, neuromodulators and neurotransmitters released upon peripheral nerve injuries activate astrocytes and microgli”
• p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “Microglia are regarded as a main source of IFMs in the CNS [12,13].”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “…syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2)…”
• Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Spinal microglia and astrocytes are both immunoeffector cells of the central nervous system that are activated following nerve injury or inflammation (104, 520, 566).”