Glial activation: a driving force for pathological pain.

By Linda R. Watkins, E. Milligan, S. Maier. Trends in Neurosciences, 2001

1,081 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/a0204964dba15dad5d8361f2d0914c25c770925d

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Citations in the corpus

Mental morbidities and chronic fatigue in severe acute respiratory syndrome survivors: long-term follow-up. (2009, background): “During acute SARS infection, cytokine storm had been demonstrated,(20) and cytokine disturbance was closely associated with somatic and painful conditions.(22) More research is needed to delineate the long-term association of endocrine status and cytokine dysfunctions with psychiatric disorders and ”
Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats (2003, background): “Although various substances are released by activated glia, proinflammatory cytokines have recently been implicated as mediators of diverse exaggerated pain states (Watkins et al., 2001).”
When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. (2011, background): “Proinflammatory cytokines can also lead to hyperalgesia and have been implicated as major contributors to chronic pain symptoms, which commonly accompany stress-related disorders (104).”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “These peripheral mediators trigger the de novo synthesis of proinflammatory cytokines by cells within the central nervous system including the spinal cord, mainly microglia, and astrocytes (324, 562, 565).”
Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord (2008, background): “Third, spinal blockade of PIC signaling attenuates chronic pain (for review, see DeLeo and Yezierski, 2001; Watkins et al., 2001).”
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, background): “…was originally thought to result exclusively from altered neuronal activity in the primary sensory and spinal cord neurons, there is evidence indicating that glial cells may also play a role in the pathogenesis of pain (Meller et al., 1994; Watkins et al., 1997, 2001a,b; DeLeo and Yezierski, 2001).”
Descending control of pain. (2002, background): “The functional status of glial cells is subject to modulation by glutamate, ACh, SP, -amino-butyric acid (GABA), 5-HT, noradrenaline (NA), adenosine and other transmitters originating in descending pathways, PAF terminals and intrinsic DH neurones (Jalonen et al., 1997; Fujita et al., 1998; Hirst et”
MAP kinase and pain (2008, background): “…previous studies focused on the responses of neurons and neuronal-specific mechanisms of hypersensitivity and chronicity of pain, accumulating evidence indicates a critical role of spinal glial cells in the pathogenesis of pain (Watkins et al., 2001; Deleo et al., 2004; Ji and Strichartz, 2004).”
Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, positive): “by microglial cells themselves or by astrocytes and T-cells.(1,3,66,76,204,348,361,362) Release of cytokines by microglia increases neuronal excitability through activation of ERK and CREB.”
ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model (2005, background): “These glial-dependent inflammatory mediators may enhance pain sensitivity in a cooperative way (DeLeo and Yezierski, 2001; Sweitzer et al., 2001; Watkins et al., 2001).”
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].”
GLIA: A novel drug discovery target for clinical pain (2003, background): “What became clear, however, was that every model tested that induced allodynia and/or hyperalgesia was associated with the activation of both astrocytes and microgli”
Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, background): “However, it is now clear that spinal cord glial cells (microglia and astroglia) importantly contribute to pain facilitation (reviewed in DeLeo and Yezierski, 2001; Watkins and Maier, 2003; Watkins et al., 2001).”
Inhibition of Microglial Activation Attenuates the Development but Not Existing Hypersensitivity in a Rat Model of Neuropathy (2003, background): “In animal models of neuropathic pain, including the L5 spinal nerve transection model, both astrocytes and micro- glia are activated, which may contribute to the development of chronic pain states (DeLeo and Yezierski, 2001; Watkins et al., 2001a,b; Raghavendra and DeLeo, 2003).”
Neural plasticity after peripheral nerve injury and regeneration. (2007, background): “In addition, spinal glial cells release proinflammatory cytokines and excitatory neuromodulators after axonal injuries, which once central sensitization is initiated, enhance the hyperexcitability of dorsal horn neurons (Watkins et al., 2001; Milligan et al., 2003; Ohtori et al., 2004).”