The neuropathic pain triad: neurons, immune cells and glia

By J. Scholz, Clifford J. Woolf. Nature Neuroscience, 2007

1,728 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/eef205b6e62a065c74df709730a3a48452e8ea1c

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Unexpected role of interferon-γ in regulating neuronal connectivity and social behavior (2016, background): “d, Both wild-type and SCID mice had an olfactory preference to urine, suggesting normal olfactory behavior (n = 8 mice per group; ANOVA for urine preference F (1, 28) = 31.”
Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain (2013, background): “Cytokines and chemokines play an important role in mediating neuroinflammation and neurodegeneration in various kinds of inflammatory neurodegenerative diseases including bacterial meningitis, brain abscesses, Lyme neuroborreliosis, and HIV encephalitis described above.”
Neural mechanism underlying acupuncture analgesia. (2008, background): “Increasing evidence has demonstrated that the mechanisms underlying pathological pain are much more complex than physiological pain (Scholz and Woolf, 2007).”
Purinergic signalling and disorders of the central nervous system (2008, background): “These observations have led to an explosion of work focused on purinergic signalling in neuropathic pai”
The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “Neutrophil recruitment is mediated by the release of chemoattractants, such as nerve growth factor-β (NGF-β), CXCL1, monocyte chemoattractant protein-1 (MCP1) and lekotriene-B4 (Johnston et al., 1999; Scholz and Woolf, 2007).”
Chronic pain may change the structure of the brain. (2008, methodology): “However, this meta-analysis will focus on the most recent studies using structural brain imaging in chronic pain patients and will not cover the other neuronal systems that have already been considered in excellent reviews [25,40,50,70,80].”
TFOS DEWS II pain and sensation report (2017, positive): “A loss of the inhibitory GABA-mediated chloride current may allow for an upregulation of ascending pain pathway signals and thus a chronic neuropathic pain state [403,404].”
Glia and pain: Is chronic pain a gliopathy? (2013, background): “Painful 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)…”
Pathological and protective roles of glia in chronic pain (2009, background): “Role of glia in pathological pain processing It is now thought that solely considering neuronal activity provides an incomplete understanding of the creation and maintenance of chronic neuropathic pai”