ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model

By Z. Zhuang, P. Gerner, Clifford J. Woolf, R. Ji. Pain, 2005

752 citations recorded by the source corpus.

Subfields: Neurology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/9cba9a6f1a202a52cf9dd54ad6ff70c115928b8e

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Citations in the corpus

p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “In addition to p38 activation in spinal microglia, we found that ERK, another MAPK family member, is also activated in spinal microglia at early times (first several days) of neuropathic pain development, which is required for neuropathic pain sensitization [ 61 ].”
MAP kinase and pain (2008, background): “Zhuang et al. (2005) also investigated ERK activation immediately after nerve injury, from 10 min to 6 h, and found that ERK is transiently activated in dorsal horn neurons.”
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”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Mechanical hyperalgesia is reduced when a high dose of an extracellular signalregulated kinase inhibitor (PD98059) is injected intrathecally on days 2, 10, or 21 (623), suggesting its involvement in maintenance of neuropathic pain.”
Pathological and protective roles of glia in chronic pain (2009, background): “Although similar pathways are activated in microglia after nerve injur”
Glia and pain: Is chronic pain a gliopathy? (2013, background): “Furthermore, prior neonatal injury can ‘‘prime’’ the spinal microglial response to adult injury, resulting in enhanced microglial reactivity [13].”
Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, neutral): “than microglia, and may play more of a role in the maintenance of neuropathic pain hypersensitivity than microglia.(94,399,406) What seems clear is that multiple different mechanisms operate after nerve injury to increase excitability and reduce inhibition.”