The DOI matches its Crossref record; 75 of the 76 references it cites were found in a registry or an index.
Neuronal Plasticity: Increasing the Gain in Pain
Abstract
We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
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In the citing paper
“Sometimes, however, central neural processing can be 'modified' so that initially peripherally induced central sensitization becomes independent of peripheral sensitization”
From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Woolf and Salter, 2000
In the citing paper
“Central sensitization is initiated by peripheral sensitization (Fig. 1) and maintained by continued input to the CNS from sensitized sensory afferent fibers”
From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Woolf and Salter, 2000
In the citing paper
“Changes in activity of peripherally sensitized fibers, due to estradiol and sympathetic modulation in the rat model, can 'modulate' activity of centrally sensitized neurons to affect pain severity”
From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Woolf and Salter, 2000
In the citing paper
“Central pain sensitization (CPS) results from neuronal plasticity that involves structural and functional changes in the central nervous system (CNS).”
From Effectiveness of acceptance and commitment therapy in central pain sensitization syndromes: A systematic review (2021) · cites this paper as [1]
Citations
Cites
The capsaicin receptor: a heat-activated ion channel in the pain pathway
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Voltage-dependent block by Mg2+ of NMDA responses in spinal cord neurones
Mayer, M. L., Westbrook, G. L., & Guthrie, P. B. (1984) · Nature · doi:10.1038/309261a0 · Cited by 2,941
Long-Term Potentiation--A Decade of Progress?
Malenka, R. C., & Nicoll, A. R. A. (1999) · Science · doi:10.1126/science.285.5435.1870 · Cited by 2,729
Neuropathic pain: aetiology, symptoms, mechanisms, and management
Woolf, C. J., & Mannion, R. (1999) · The Lancet · doi:10.1016/s0140-6736(99)01307-0 · Cited by 2,231
Evidence for a central component of post-injury pain hypersensitivity
Woolf, C. J. (1983) · Nature · doi:10.1038/306686a0 · Cited by 2,157
A capsaicin-receptor homologue with a high threshold for noxious heat
Caterina, M. J., Rosen, T. A., Tominaga, M., Brake, A. J., & Julius, D. J. (1999) · Nature · doi:10.1038/18906 · Cited by 1,599
Peripheral nerve injury triggers central sprouting of myelinated afferents
Woolf, C. J., Shortland, P. J., & Coggeshall, R. E. (1992) · Nature · doi:10.1038/355075a0 · Cited by 1,083
The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways
Akopian, A. N., Souslova, V., England, S. G., Okuse, K., Ogata, N., Ure, J. M., Smith, A., Kerr, B. J., McMahon, S. B., Boyce, S., et al. (1999) · Nature Neuroscience · doi:10.1038/9195 · Cited by 828
Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity
Ji, R., Baba, H., Brenner, G. J., & Woolf, C. J. (1999) · Nature Neuroscience · doi:10.1038/16040 · Cited by 787
Messenger plasticity in primary sensory neurons following axotomy and its functional implications
Hökfelt, T. G. M., Zhang, X., & Wiesenfeld‐Hallin, Z. (1994) · Trends in Neurosciences · doi:10.1016/0166-2236(94)90031-0 · Cited by 742
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Cited by
Sorted by citations
Central sensitization: implications for the diagnosis and treatment of pain
Woolf, C. J. (2011) · Pain · doi:10.1016/j.pain.2010.09.030 · Cited by 4,771
Persistent postsurgical pain: risk factors and prevention
Kehlet, H., Jensen, T. S., & Woolf, C. J. (2006) · The Lancet · doi:10.1016/s0140-6736(06)68700-x · Cited by 4,086
Central sensitization: a generator of pain hypersensitivity by central neural plasticity
Latremoliere, A., & Woolf, C. J. (2009) · The Journal of Pain · doi:10.1016/j.jpain.2009.06.012 · Cited by 3,913
“as large low-threshold mechanoreceptor myelinated fibers to produce Ab fiber–mediated pain.(376) It also produces pain hypersensitivity in noninflamed tissue by changing the sensory response elicited by normal inputs”
InfluentialSelf-citationGlutamate Receptor Ion Channels: Structure, Regulation, and Function
Traynelis, S. F., Wollmuth, L. P., McBain, C. J., Menniti, F. S., Vance, K. M., Ogden, K. K., Hansen, K. B., Yuan, H., Myers, S. J., & Dingledine, R. (2010) · Pharmacological Reviews · doi:10.1124/pr.109.002451 · Cited by 3,568
Molecular mechanisms of nociception
Julius, D., & Basbaum, A. I. (2001) · Nature · doi:10.1038/35093019 · Cited by 2,685
“Moreover, because expression of neurotransmitters, their receptors and other signalling molecules are dramatically altered after tissue or nerve injur”
Background
Metadata
- Authors
- Woolf, C. J., & Salter, M. W.
- Affiliations
- Harvard University (US)
- University of Toronto (CA)
- Corresponding author
- Woolf, Clifford J.
- Venue
- Science
- Published
- 2000-06-09
- Volume
- 288
- Issue
- 5472
- Pages
- 1765-1768
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2133316133
- Cited by
- 3,781
- References
- 76
- Citations by year
- 2026: 62 · 2025: 101 · 2024: 96 · 2023: 104 · 2022: 99 · 2021: 99 · 2020: 129 · 2019: 112 · 2018: 124 · 2017: 140 · 2016: 150 · 2015: 170 · 2014: 142 · 2013: 188 · 2012: 166
- FWCI
- 13.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- neuroplasticity, pain, hyperalgesia, primary sensory neurons, dorsal horn neurons, neuropathic pain, inflammatory pain, plasticity mechanisms, pain modulation
- MeSH terms
- Animals, Humans, Inflammation, Models, Neurological, Synaptic Transmission, Neuronal Plasticity, Neurons, Afferent, Nociceptors, Pain, Signal Transduction, Posterior Horn Cells, Peripheral Nerve Injuries
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