Central sensitization and LTP: do pain and memory share similar mechanisms?

By R. Ji, T. Kohno, K. Moore, Clifford J. Woolf. Trends in Neurosciences, 2003

1,476 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/18b80298d5f8ba4532d9df475ed9ea1f2003cc7a

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. R. Ji
2. M. Suter
3. Clifford J. Woolf
4. Z. Zhuang
5. P. Gerner
6. S. Cooke
7. T. Bliss
8. R. Meyer

In Molecular Biology

1. Clifford J. Woolf
2. R. Ji
3. M. Suter
4. R. Kuner
5. S. Cooke
6. T. Bliss
7. R. Meyer
8. J. Campbell

In Physiology

1. Clifford J. Woolf
2. R. Ji
3. M. Suter
4. Z. Zhuang
5. T. Berta
6. Maiken Nedergaard
7. M. Malcangio
8. P. Gerner

Citations in the corpus

• Plasticity in the human central nervous system. (2006, methodology): “This model has enabled the identification of cell types and signalling pathways involved in long-lasting central sensitization (reviewed in Han, 2003), and has also suggested the involvement of synaptic LTP in the induction of hyperalgesia (reviewed in Ji et al., 2003).”
• p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “AMPA and NMDA currents) or/and a reduction in inhibitory synaptic transmission (e.g. GABA currents) [ 7-9 ].”
• 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): “Increased synaptic transmission in dorsal horn neurons, central sensitization, has been strongly implicated in persistent pain development (Woolf and Salter, 2000; Ji et al., 2003).”
• Daily Assessment of Pain in Adults with Sickle Cell Disease (2008, background): “Some propose a special cause of hyperalgesia known as central sensitization—central nervous system neuroreceptive pain, even without a continuing local pain stimulus (26)—as a cause of chronic pain in sickle cell disease (13).”
• Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury (2006, background): “, 2003), which have been implicated in the induction of central sensitization of spinal neurons (Palecek et al., 1994; Minami et al., 1999; Samad et al., 2001; Ji et al., 2003).”
• 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): “(Impey et al., 1999; Ji and Woolf, 2001; Ji et al., 2003; Widmann et al., 1999).”
• Central sensitization: Implications for the diagnosis and treatment of pain (2010, background): “phenomena converge in this, and in other model systems, although there are differences too [122,274].”
• MAP kinase and pain (2008, background): “pivotal for long-term neuronal plasticity in both hippocampal and dorsal horn neurons (Ji et al., 2003).”
• Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management (2004, background): “Later, it is sustained beyond the initiating stimulus by transcriptional changes in the molecular machinery of the cell (that is, it becomes transcription dependent) (Figure 3C) (14, 33).”
• Central mechanisms of pathological pain (2010, background): “Diverse molecules modulate spinal pain processing by activating cell surface receptors in discrete spatial and temporal pattern”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “Finally, the proinflammatory cytokines TNF-a, IL-1b, and IL-6 also elicit long-term neuronal plasticity in the pain circuit by inducing the phosphorylation of the transcription factor cAMP response element-binding protein (CREB), leading to the transcription of CREB-mediated pronociceptive genes (eg”
• Mechanisms of neuropathic pain. (2006, background): “Ample evidence indicates that heterosynaptic and homosynaptic sensitization occur in neuropathic pain conditions (Campbell et al., 1988; Ji et al., 2003).”
• Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, neutral): “spatial extent of their input, and changes that outlast an initiating trigger.(132,368,369,372,376) These electrophysiological changes correlate remarkably with the n: Generator of Pain Hypersensitivity by Central Neural Plasticity”