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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“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]
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“It is known that elevation of intracellular calcium activates several protein kinases, such as protein kinase C and calcium/calmodulin-dependent protein kinase II. Activation of these protein kinases leads to the phosphorylation of ionotropic glutamate receptors, increasing synaptic efficacy ( Woolf and Salter, 2000;…”
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Neuropathic changes in equine laminitis pain
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“After synaptic transmission and modulation within the sensory neuron and spinal cord, nociceptive signals reach the brain, where they are finally perceived as ‘‘pain,’’ within the context of cognitive and environmental factors (Woolf and Salter 2000).”
Stapleton, F. J., Marfurt, C. F., Golebiowski, B., Rosenblatt, M. I., Bereiter, D. A., Begley, C. G., Dartt, D. A., Gallar, J., Belmonte, C., Hamrah, P., et al. (2013) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.13-13226 · Cited by 104
“The past decade has seen marked advances in elucidating the dynamic nature of pain and the mechanisms involved in its transition from an acute physiological and protective state to a persistent and often deleterious state (see the studies by Woolf and Salter 398 and by Basbaum and colleagues 68 ).”
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“Peripheral inflammation causes both a central sensitization, caused by the release of glutamate and neuropeptides from primary afferent nociceptors in lamina II (Millan, 1999; Woolf and Salter, 2000), and the activation of glial cells in the DH (Watkins et al., 2001).”
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Nesic, O., Svrakic, N. M., Xu, G., McAdoo, D. J., Westlund, K. N., Hulsebosch, C. E., Ye, Z., Galante, A., Soteropoulos, P., Tolias, P. P., et al. (2002) · Journal of Neuroscience Research · doi:10.1002/jnr.10171 · Cited by 102
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“Central sensitization plays a pivotal role in the switch from acute to chronic pain mechanisms [5,6] and the”
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“Chronic pain is most often associated with neuroplastic changes of the central nervous system (CNS) [1,2].”
BackgroundWhite matter microstructural alterations in migraine: A diffusion-weighted MRI study
Szabó, N., Kincses, Z. T., Párdutz, Á., Tajti, J., Szok, D., Tuka, B., Király, A., Babos, M., Vörös, E., Bomboi, G., et al. (2012) · Pain · doi:10.1016/j.pain.2011.11.029 · Cited by 105
“Explanation of such controversy may lie in a lack of noxious stimulus in chronic pain [53], chronification of the pain condition, compensatory mechanisms [79] or affective components [36], and personality traits related to migraine [12].”
BackgroundExpression of IL-1β in supraspinal brain regions in rats with neuropathic pain
Apkarian, A. V., Lavarello, S., Randolf, A., Berra, H. H., Chialvo, D. R., Besedovsky, H. O., & del Rey, A. (2006) · Neuroscience Letters · doi:10.1016/j.neulet.2006.08.034 · Cited by 103
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“2 potassium channels(17,19) and by contributing to the phosphorylation of the NR1 subunit of N-methylD-aspartate (NMDA) receptors,(43)whichare essential for the induction of central sensitization.(49) ERK also plays a role in transcriptional”
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Translational Pain Research: Achievements and Challenges
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“Activation of nociceptors in the periphery produces messages which converge in the dorsal horn of the spinal cord which process the nociceptive information and project it to the cerebral cortex via a relay in the thalamus, eliciting pain [38].”
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Migraine and the neck: New insights from basic data
Bartsch, T. (2005) · Current Pain and Headache Reports · doi:10.1007/s11916-005-0061-0 · Cited by 102
“The hypersensitivity of the afferent synaptic input in the spinal cord is thought to be due to the stimulation-induced release of various neuropeptides, such as calcitonin gene-related peptide, or to glutamate release and action at the N-methyl-D-aspartate receptor, but also may be due to a decrease of local segmental…”
BackgroundPain management in trauma: A review study
Ahmadi, A., Bazargan‐Hejazi, S., Zadie, Z. H., Euasobhon, P., Ketumarn, P., Karbasfrushan, A., Saman, J. A., & Mohammadi, R. (2016) · Journal of Injury and Violence Research · doi:10.5249/jivr.v8i2.707 · Cited by 102
Grain‐Boundary Engineering of Monolayer MoS 2 for Energy‐Efficient Lateral Synaptic Devices
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Classification of low back-related leg pain—A proposed patho-mechanism-based approach
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The role of nucleotides in the neuron–glia communication responsible for the brain functions
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Effects of low‐dose intranasal (S)‐ketamine in patients with neuropathic pain
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The Measurement of Pain in Infants, Children, and Adolescents: From Policy to Practice
O’Rourke, D. (2004) · Physical Therapy · doi:10.1093/ptj/84.6.560 · Cited by 102
Glycine transporter inhibitors as a novel drug discovery strategy for neuropathic pain
Dohi, T., Morita, K., Kitayama, T., Motoyama, N., & Morioka, N. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.03.018 · Cited by 100
Sensory hypoaesthesia is a feature of chronic whiplash but not chronic idiopathic neck pain
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“The duration of the nociceptive input is another factor thought to play an important role in maintaining CNS hyperexcitability (Rang et al., 1991; Woolf and Salter, 2000).”
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“The long-lasting nociceptive transmission under various pathological chronic pain conditions involve transcriptional and/or translational alteration in neurotransmitter and receptor expression as well as modification of neuronal function, morphology, and synaptic connections [11,13,46,48].”
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“Plasticity in peripheral nociceptors and their synapses with spinal neurons has been proposed as a cellular basis for the development and maintenance of pain hypersensitivity following peripheral inflammation or nerve injury [1–3].”
Anti-allodynic efficacy of botulinum neurotoxin A in a model of neuropathic pain
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“Aside from analgesic efficacy, the antihyperalgesic effect of magnesium could be clinically relevant because opioid-induced hyperalgesia may be one of the potential risk factors for the development of chronic pain after major surgery such as thoracotomy or laparotomy.(9) –12 Adverse events related to the administratio…”
ResultAge-related changes in the spinal cord microglial and astrocytic response profile to nerve injury
Vega‐Avelaira, D., Moss, A., & Fitzgerald, M. (2006) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2006.10.007 · Cited by 100
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“Supra-spinal mechanisms of pain may lead to neuroplastic changes in the brain structures participating in the processing of noxious information (Woolf and Salter, 2000).”
BackgroundThe Rationale and Use of Topiramate for Treating Neuropathic Pain
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“This concept is based on the pathophysiology of surgical pain, including peripheral sensitization, which is a reduction in the threshold of nociceptor afferent peripheral terminals initiated by inflammatory mediators, and central sensitization, which is hyperexcitability of the spinal neurons in the dorsal horn [3, 4,…”
BackgroundLiu, M., & Chen, J. (2014) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2014.01.003 · Cited by 101
Sterling, M. M. (2010) · Pain · doi:10.1016/j.pain.2010.06.003 · Cited by 99
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Reduction of Postincisional Allodynia by Subcutaneous Bupivacaine
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“The plasma lifetime of bupivacaine in rats is less than 6 h,(20) so the week-long effects are the consequence of actions that occur in the perioperative period, when afferent discharge from injured nerves is most robust and acute spinal sensitization is first induced.(32) Interestingly, the initial increase in primary…”
Molecular Bases of Caloric Restriction Regulation of Neuronal Synaptic Plasticity
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“Also, changes in neurotransmission of nociceptive neurons in the dorsal horn of the spinal cord seems to be required for the modulation of some forms of pain [36, 37].”
BackgroundFunctional brain imaging of trigeminal neuralgia
Moisset, X., Villain, N., Ducreuxl, D., Serriel, A., Cuninl, G., Valadel, D., Calvinol, B., & Bouhassiral, D. (2010) · European Journal of Pain · doi:10.1016/j.ejpain.2010.06.006 · Cited by 99
Systemic inflammation impairs respiratory chemoreflexes and plasticity
Huxtable, A. G., Vinit, S., Windelborn, J. A., Crader, S. M., Guenther, C. H., Watters, J. J., & Mitchell, G. S. (2011) · Respiratory Physiology & Neurobiology · doi:10.1016/j.resp.2011.06.017 · Cited by 99
NO Pain: Potential Roles of Nitric Oxide in Neuropathic Pain
Levy, D., & Zochodne, D. W. (2004) · Pain Practice · doi:10.1111/j.1533-2500.2004.04002.x · Cited by 99
Nijs, J., Wijma, A. J., Willaert, W., Huysmans, E., Mintken, P., Smeets, R., Goossens, M., van Wilgen, C. P., Van Bogaert, W., Louw, A., et al. (2020) · Physical Therapy · doi:10.1093/ptj/pzaa021 · Cited by 97
Altered structure and functional connection in patients with classical trigeminal neuralgia
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“On the other hand, central sensitization or use-dependent synaptic plasticity can occur when there is the sustained or repetitive activation of nociceptive afferent fibers [DeSouza et al., 2016; Woolf, 2010].”
BackgroundWhat is the Role of NSAIDs in Pre-emptive Analgesia?
Ochroch, E. A., Mardini, I. A., & Gottschalk, A. (2003) · Drugs · doi:10.2165/00003495-200363240-00002 · Cited by 98
Ramer, L. M., Borisoff, J., & Ramer, M. S. (2004) · Journal of Neuroscience · doi:10.1523/jneurosci.3337-04.2004 · Cited by 98
“Alternate mechanisms for the development of cold hyperalgesia involve increases in the excitability in the peripheral terminals of cold-sensitive neurons and/or increases in the sensitivity of higher-order neurons to glutamate (Woolf and Salter, 2000).”
BackgroundHLA-B62 and HLA-DQ8 are associated with Complex Regional Pain Syndrome with fixed dystonia
A, A. M. D. R., Gosso, F. M., Haasnoot, G. W., Marinus, J., Verduijn, W., Claas, F. H. J., van den Maagdenberg, A. M. J. M., & van Hilten, J. J. (2009) · Pain · doi:10.1016/j.pain.2009.05.015 · Cited by 98
“Neuroplasticity is a process whereby neurons reorganize their connectivity in response to altered experiences like injury [37,38].”
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Stress-Induced Chronic Visceral Pain of Gastrointestinal Origin
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“Typically the nociceptors use glutamatergic signaling, to activate ionotropic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors on the target neuron, with co-release of neuromodulators, such as substance P, to activate similar second-messenger systems to modulate the…”
BackgroundPedersen, L. H., Nielsen, A. N., & Blackburn-Munro, G. (2005) · Psychopharmacology · doi:10.1007/s00213-005-0120-6 · Cited by 97
“infection, metabolic disturbance or direct physical insult induces plasticity changes within the dorsal horn, which underlie central sensitisation and manifest behaviourally as allodynia and hyperalgesia (Woolf and Salter 2000; Blackburn-Munro 2004).”
BackgroundMaladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury
Ferguson, A. R., Huie, J. R., Crown, E. D., Baumbauer, K. M., Hook, M. A., Garraway, S. M., Lee, K. H., Hoy, K. C., & Grau, J. W. (2012) · Frontiers in Physiology · doi:10.3389/fphys.2012.00399 · Cited by 98
“This increase in spinal activity, known as “central sensitization,” reflects a form of neuroplasticity in the spinal cord (Woolf and Salter, 2000).”
BackgroundPharmacology of systemic analgesics
Camu, F., & Vanlersberghe, C. (2002) · Best practice & research. Clinical anaesthesiology · doi:10.1053/bean.2002.0262 · Cited by 97
Sodium channels in pain disorders: pathophysiology and prospects for treatment
Dib‐Hajj, S. D., Geha, P., & Waxman, S. G. (2017) · Pain · doi:10.1097/j.pain.0000000000000854 · Cited by 103
“More than half a century of animal research in the setting of a peripheral injury has now extensively described the neural nociceptive machinery that transmits information about potentially painful stimuli cephalad and demonstrates its plasticity in animal models of pain.(119,120) However, conditions such as fibromyal…”
Ma, W., & Quirion, R. (2001) · Pain · doi:10.1016/s0304-3959(01)00335-9 · Cited by 96
“These changes trans-synaptically affect second relay neurons of the nociceptive pathway (Woolf and Salter, 2000).”
BackgroundThe Incidence of Mechanical Allodynia in Patients With Irreversible Pulpitis
Owatz, C. B., khan, A. W. A., Schindler, W. G., Schwartz, S. A., Keiser, K., & Hargreaves, K. (2007) · Journal of Endodontics · doi:10.1016/j.joen.2007.01.023 · Cited by 96
Human cerebellar responses to brush and heat stimuli in healthy and neuropathic pain subjects
Borsook, D., Moulton, E. A., Tully, S., Schmahmann, J. D., & Becerra, L. R. (2008) · The Cerebellum · doi:10.1007/s12311-008-0011-6 · Cited by 96
Extracellular High-Mobility Group Box 1 Protein (HMGB1) as a Mediator of Persistent Pain
Agalave, N. M., & Svensson, C. I. (2014) · Molecular Medicine · doi:10.2119/molmed.2014.00176 · Cited by 99
New Treatments for Reflex Sympathetic Dystrophy
Schwartzman, R. J. (2000) · New England Journal of Medicine · doi:10.1056/nejm200008313430911 · Cited by 96
Duan, B., Liu, D.-S., Huang, Y., Zeng, W.-Z., Wang, X., Yu, H., Zhu, M. X., Chen, Z.-Y., & Xu, T. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.4479-11.2012 · Cited by 97
“Functional effects of BDNF on pain-signaling pathways The neurotrophin BDNF acts as a central modulator of pain via PKC/ERK pathways (Woolf and Salter, 2000; Pezet and McMahon, 2006).”
BackgroundCortical disinhibition occurs in chronic neuropathic, but not in chronic nociceptive pain
Schwenkreis, P., Scherens, A., Rönnau, A.-K., Höffken, O., Tegenthoff, M., & Maier, C. (2010) · BMC Neuroscience · doi:10.1186/1471-2202-11-73 · Cited by 102
“This different activation of the nociceptive system leads to differential plastic changes at the level of primary sensory and dorsal horn neurons [32].”
BackgroundHasenbring, M. I., Chehadi, O., Titze, C., & Kreddig, N. (2014) · Pain Management · doi:10.2217/pmt.14.36 · Cited by 106
Brain dynamics for perception of tactile allodynia (touch-induced pain) in postherpetic neuralgia
Geha, P., Baliki, M. N., Wang, X., Harden, R. N., Paice, J. A., & Apkarian, A. V. (2008) · Pain · doi:10.1016/j.pain.2008.02.021 · Cited by 94
“On the other hand, we also hypothesize that brain activity for allodynia and spontaneous pain should show minimal overlap, mainly because animal studies [16,19,65], and human studies [43], indicate that distinct afferent fiber types and spinal cord processes mediate these perceptions.”
ResultHayashida, K., Clayton, B. A., Johnson, J. E., & Eisenach, J. C. (2007) · Pain · doi:10.1016/j.pain.2007.07.014 · Cited by 95
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“There is compelling evidence demonstrating that hyperalgesia, allodynia, and ongoing pain associated with peripheral nerve injury reflect, at least in part, changes in the excitability of primary afferent neurons (Suzuki and Dickenson, 2000; Woolf and Salter, 2000; Zimmermann, 2001).”
BackgroundRole of delivery and trafficking of δ-opioid peptide receptors in opioid analgesia and tolerance
Zhang, X., Bao, L., & Guan, J. (2006) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2006.04.005 · Cited by 95
“These changes in tachykinin expression could modulate the size of the intracellular pool of DOP receptors for stimulus-induced delivery (Figure 2). Nerve growth factor might be important for DOP receptor regulation in nociceptive sensory neurons because it is responsible for regulating the expression of substance P in…”
BackgroundInfluentialPathophysiology and treatment of neuropathic pain associated with syringomyelia
Rusbridge, C., & Jeffery, N. D. (2007) · The Veterinary Journal · doi:10.1016/j.tvjl.2006.12.007 · Cited by 97
Therapeutic implications of central and peripheral neurologic mechanisms in migraine
Waeber, C., & Moskowitz, M. A. (2003) · Neurology · doi:10.1212/wnl.61.8_suppl_4.s9 · Cited by 95
Cough, pain and dyspnoea: Similarities and differences
Gracely, R. H., Undem, B. J., & Banzett, R. B. (2007) · Pulmonary Pharmacology & Therapeutics · doi:10.1016/j.pupt.2006.12.005 · Cited by 93
“Among the mechanisms that may underlie allodynia is central sensitization of afferent pain pathways caused by converging nociceptor input; this has been well described in many experimental systems [9,10].”
The burden of acute postoperative pain and the potential role of the COX-2-specific inhibitors
Stephens, J. M. L. (2003) · British journal of rheumatology · doi:10.1093/rheumatology/keg497 · Cited by 95
“Chronic pain generally arises as a result of neuronal plasticity following protracted central nervous system hyperexcitability [7, 33, 34], and it has been suggested that appropriate analgesic therapy, such as pre-emptive analgesia, prevents the establishment of central sensitization [35].”
BackgroundPathophysiology of Pain and Mechanisms of Neuromodulation: A Narrative Review (A Neuron Project)
Karcz, M., Abd-Elsayed, A. A., Chakravarthy, K. V., Aman, M. M., Strand, N. H., Malinowski, M. N., Latif, U., Dickerson, D. M., Suvar, T., Lubenow, T. R., et al. (2024) · Journal of Pain Research · doi:10.2147/jpr.s475351 · Cited by 130
Protein Kinases as Potential Targets for the Treatment of Pathological Pain
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Memory Traces of Pain in Human Cortex
Albanese, M., Duerden, E. G., Rainville, P., & Duncan, G. H. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.0695-07.2007 · Cited by 92
“, 2004), and the transformation of acute peripheral injury to centralized chronic pain (Woolf and Salter, 2000).”
BackgroundCharrier, C., Machado, P., Tweedie‐Cullen, R. Y., Rutishauser, D., Mansuy, I. M., & Triller, A. (2010) · Nature Neuroscience · doi:10.1038/nn.2645 · Cited by 100
“These regulations may be crucial in vivo for the modulation of pain pathway”
BackgroundPlastic Changes in Nociceptive Transmission of the Rat Spinal Cord With Advancing Age
Iwata, K., Fukuoka, T., Kondo, E., Tsuboi, Y., Tashiro, A., Noguchi, K., Masuda, Y., Morimoto, T., & Kanda, K. (2002) · Journal of Neurophysiology · doi:10.1152/jn.00243.2001 · Cited by 94
p38 mitogen-activated protein kinase and pain
Mai, L., Zhu, X. M., Huang, F., He, H., & Fan, W. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.117885 · Cited by 93
Physiological Mechanisms Of Neuropathic Pain: The Orofacial Region
Iwata, K., Imamura, Y., Honda, K., & Shinoda, M. (2011) · International review of neurobiology · doi:10.1016/b978-0-12-385198-7.00009-6 · Cited by 93
Borsook, D., Burstein, R., & Becerra, L. R. (2004) · Journal of Neurobiology · doi:10.1002/neu.20085 · Cited by 93
Lang, S., Klein, T., Magerl, W., & Treede, R. (2006) · Pain · doi:10.1016/j.pain.2006.09.026 · Cited by 93
“Thus, LTP has joined segmental inhibition and descending inhibition and facilitation in the list of potential mechanisms that modulate nociceptive pathways (Woolf and Salter, 2000; Ji et al., 2003).”
BackgroundDoes past pain influence current pain: biological and psychosocial models of sex differences
Rollman, G. B., Abdel‐Shaheed, J., Gillespie, J. M., & Jones, K. S. (2004) · European Journal of Pain · doi:10.1016/j.ejpain.2004.03.002 · Cited by 99
Clinical diagnosis and treatment of suspected neuropathic pain in three dogs
Cashmore, R. G., Harcourt‐Brown, T., Freeman, P., Jeffery, N. D., & Granger, N. P. (2009) · Australian Veterinary Journal · doi:10.1111/j.1751-0813.2008.00379.x · Cited by 93
Burstein, R., Jakubowski, M., & Rauch, S. D. (2011) · Journal of Vestibular Research · doi:10.3233/ves-2012-0433 · Cited by 92
“CGRP and SP are thought to sensitize nociceptors indirectly by inducing the release of sensitizing inflammatory mediators such as histamine, 5HT, BK, TNF-alpha and nitric oxide from other immune cells, especially mast cells, in a process known as mast cell degranulation [77,94,112].”
BackgroundNeuropathic Pain in Dogs and Cats: If Only They Could Tell Us If They Hurt
Mathews, K. A. (2008) · Veterinary Clinics of North America Small Animal Practice · doi:10.1016/j.cvsm.2008.09.001 · Cited by 92
“Pain can be divided into three categories: physiologic, inflammatory, and neuropathic.(35,46,54,60)”
BackgroundEstrogen and Visceral Nociception at the Level of Primary Sensory Neurons
Chaban, V. V. (2011) · Pain Research and Treatment · doi:10.1155/2012/960780 · Cited by 92
“A decade ago, ATP was shown to be an extracellular signal involved in peripheral hyperalgesia [34].”
BackgroundGlutamate receptors and persistent pain: targeting forebrain NR2B subunits
Zhuo, M. (2002) · Drug Discovery Today · doi:10.1016/s1359-6446(01)02138-9 · Cited by 92
Glutamate receptor phosphorylation and trafficking in pain plasticity in spinal cord dorsal horn
Liu, X. J., & Salter, M. W. (2010) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2010.07351.x · Cited by 94
Melemedjian, O. K., Tillu, D. V., Asiedu, M. N., Mandell, E. K., Moy, J. K., Blute, V. M., Taylor, C. J., Ghosh, S., & Price, T. J. (2013) · Molecular Pain · doi:10.1186/1744-8069-9-12 · Cited by 93
“; licensee BioMed C Creative Commons Attribution License (http:/ distribution, and reproduction in any medium implicated in the initiation of pain in preclinical models [1-6], our understanding of molecular mechanisms that maintain chronic pain states remains poor.”
BackgroundLevene, J. L., Weinstein, E. J., Cohen, M. S., Andreae, D. A., Chao, J. Y., Johnson, M., Hall, C. B., & Andreae, M. H. (2019) · Journal of Clinical Anesthesia · doi:10.1016/j.jclinane.2018.12.043 · Cited by 96
“[5,10,21] Woolf et al explained the transition from acute to chronic pain after surgery with central sensitization (Graphical Abstract).[3,22,23] Many have since contributed to elucidate the precise molecular mechanisms.”
BackgroundThe Modification of Cortical Reorganization and Chronic Pain by Sensory Feedback
Flor, H. (2002) · Applied Psychophysiology and Biofeedback · doi:10.1023/a:1016204029162 · Cited by 91
Immediate reduction in temporal sensory summation after thoracic spinal manipulation
Bishop, M. D., Beneciuk, J. M., & George, S. Z. (2011) · The Spine Journal · doi:10.1016/j.spinee.2011.03.001 · Cited by 91
“Windup is activity-dependent modulation of dorsal horn activity [33] characterized by a progressive increase in output from dorsal horn neurons in response to repeated unchanging low-frequency nociceptor stimuli [33,34].”
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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