p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia.

By R. Ji, T. Samad, Shan-xue Jin, Raymond Schmoll, Clifford J. Woolf. Neuron, 2002

1,233 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/ba9bdfa8c08dc52f507c7c9c4e0a7c6e478bc2d6

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In Cellular and Molecular Neuroscience

In Physiology

In Sensory Systems

Citations in the corpus

p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “p38 inhibitor was shown to effectively alleviate rheumatoid arthritis and inflammatory pain [31-33].”
MAP kinase and pain (2008, background): “Furthermore, intrathecal injection of MEK inhibitors has been shown to inhibit inflammatory heat hyperalgesia and mechanical allodynia following hindpaw injection of CFA (Ji et al., 2002a; Adwanikar et al., 2004), bee venom (Yu and Chen, 2005), and scorpion venom (Pang et al., 2008), after joint mon”
Cellular and Molecular Mechanisms of Pain (2009, neutral): “8 voltage-gated sodium channel subunit (Chao, 2003; Ji et al., 2002).”
Central sensitization: Implications for the diagnosis and treatment of pain (2010, neutral): “nisms, time courses and presentations [53,97,121,123,160,171, 189,229,242,261,269].”
Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury (2006, background): “, 2005) and DRG neurons (Ji et al., 2002; Kim et al., 2002), although its precise role in activation of microglia remains uncertain.”
Distinct expression of TRPM8, TRPA1, and TRPV1 mRNAs in rat primary afferent neurons with aδ/c‐fibers and colocalization with trk receptors (2005, background): “However, the upregulation of TRPV1 mRNA in peripheral inflammation models is still controversial (Sanchez et al., 2001; Tohda et al., 2001; Ji et al., 2002; Amaya et al., 2003; Bar et al., 2004; Luo et al., 2004), and partial nerve injury increases TRPV1 mRNA mainly in TrkA-negative DRG neurons…”
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 (2003, methodology): “Double staining of p-p38 with neurofilament-200 (NF-200), a marker for myelinated A-fibers, showed no colocalization in naive control DRGs, as reported previously ( Ji et al., 2002b ).”
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).”
ANKTM1, a TRP-like channel expressed in nociceptive neurons, is activated by cold temperatures. (2003, background): “This amino acid similarity is likely significant shown to upregulate TRPV1 mRNA and protein in culat the structural level since ruthenium red, a potent tured DRG neurons (Chuang et al., 2001; Ji et al., 2002; blocker of TRPV channels, also blocks ANKTM1.”
Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management (2004, background): “For example, after peripheral inflammation, there is an increase in the level of the heat-sensitive transient receptor potential V1 channel in the peripheral terminal of nociceptors, increasing peripheral sensitivity to heat (29), and in levels of the synaptic modulators substance P and brain-derive”