The role of neuroinflammation and neuroimmune activation in persistent pain

By J. Deleo, R. Yezierski. Pain, 2001

636 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/e5f063bffaf5076ba992e4e34f5e8b709911974f

How researchers see this paper

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

In Developmental Neuroscience

1. R. Ji
2. M. Millan
3. Clifford J. Woolf
4. S. Maier
5. Maiken Nedergaard
6. E. Milligan
7. Linda R. Watkins

In Physiology

1. Clifford J. Woolf
2. R. Ji
3. M. Suter
4. Linda R. Watkins
5. E. Milligan
6. Z. Zhuang
7. S. Maier
8. G. Moalem-Taylor

In Surgery

1. R. Ji
2. M. Millan
3. Clifford J. Woolf
4. Maiken Nedergaard

Citations in the corpus

• 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): “Although pain hypersensitivity 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,”
• 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).”
• Descending control of pain. (2002, background): “The latter can infiltrate the DH following damage to the spinal cord, to PAFs or to peripheral tissue, events provoking a loss of blood–brain barrier integrity (Millan, 1999; Watkins and Maier, 1999a,b; Bezzi and Volterra, 2001; DeLeo and Yezierski, 2001).”
• Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, neutral): “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.”
• Curcumin and cancer: an "old-age" disease with an "age-old" solution. (2008, background): “Curcumin inhibited the IL-6 production, histone acetyltransferase (HAT) activity, and AP-1 activation [38] and prevented cell death and apoptotic biochemical changes, such as the mitochondrial release of cytochrome c, the activation of caspase3, and the cleavage of PARP in human hepatoma cells [7,39”
• 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).”
• 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).”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “matory, neuropathic, and caner pain and morphine tolerance [52,213,230,273].”
• Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness. (2008, neutral): “It is already known that microglia release neuroexcitatory substances in response to morphine, thereby opposing its effects [19, 122, 123, 124].”
• Central sensitization and LTP: do pain and memory share similar mechanisms? (2003, background): “A further source of IL-1b and other cytokines in the CNS is recruitment and activation of microglia [ 84 ].”
• 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 MAPK, microglial signaling, and neuropathic pain (2007, background): “All of these IFMs are implicated in pain facilitation [13-17,44,54,55].”