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MeSH Review


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Disease relevance of Hyperalgesia


Psychiatry related information on Hyperalgesia


High impact information on Hyperalgesia


Chemical compound and disease context of Hyperalgesia

  • Here we present a new model for noradrenaline-sensitive hyperalgesia and demonstrate that the site of action of noradrenaline is not on the primary afferents but rather is presynaptic on the sympathetic post-ganglionic terminals [16].
  • NSAIDs are now shown to exert a direct spinal action by blocking the excessive sensitivity to pain (hyperalgesia) induced by the activation of spinal glutamate and substance P receptors [17].
  • This diet-induced hyperalgesia can be reversed by feeding the animals diets with adequate amounts of tryptophan, or by systemic injections of the amino acid [18].
  • There is compelling evidence linking bradykinin (BK) with the pathophysiological processes that accompany tissue damage and inflammation, especially the production of pain and hyperalgesia [19].
  • Spinal inflammatory hyperalgesia is mediated by prostaglandin E receptors of the EP2 subtype [20].
  • In pain and opioid-experienced rats, NMDA receptor antagonists, ketamine or BN2572, completely prevented hyperalgesia when injected just before NNES or fentanyl ULD [21].
  • 4 days of dexamethasone as well as doxantrazole diminished the SLIGRL-induced hyperalgesia for all volumes of distension [22].

Biological context of Hyperalgesia


Anatomical context of Hyperalgesia


Gene context of Hyperalgesia

  • We have delineated the region of IL-1 beta mediating the hyperalgesic effect and developed an analgesic tripeptide analogue of IL-1 beta which antagonizes hyperalgesia evoked by IL-1 beta and by the inflammatory agent carrageenan [31].
  • After a peripheral inflammatory stimulus, EP2-/- mice exhibit only short-lasting peripheral hyperalgesia but lack a second sustained hyperalgesic phase of spinal origin [20].
  • This process, called sensitization or hyperalgesia, is mediated by a variety of proinflammatory factors, including bradykinin, ATP and NGF, which cause sensitization to noxious heat stimuli by enhancing the membrane current carried by the heat- and capsaicin-gated ion channel, TRPV1 [32].
  • We conclude that when unopposed by NA, substance P acting at the NK1 receptor causes chronic thermal hyperalgesia, and that the reduced opioid efficacy associated with a lack of NA is due to increased NK1-receptor stimulation [33].
  • Therapeutic or prophylactic administration of SC-560 in the rat carrageenan footpad model did not affect acute inflammation or hyperalgesia at doses that markedly inhibited in vivo COX-1 activity [34].

Analytical, diagnostic and therapeutic context of Hyperalgesia


  1. Relation between sympathetic vasoconstrictor activity and pain and hyperalgesia in complex regional pain syndromes: a case-control study. Baron, R., Schattschneider, J., Binder, A., Siebrecht, D., Wasner, G. Lancet (2002) [Pubmed]
  2. Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. Nemeroff, C.B., Osbahr, A.J., Manberg, P.J., Ervin, G.N., Prange, A.J. Proc. Natl. Acad. Sci. U.S.A. (1979) [Pubmed]
  3. Kappa- and delta-opioids block sympathetically dependent hyperalgesia. Taiwo, Y.O., Levine, J.D. J. Neurosci. (1991) [Pubmed]
  4. Gene transfer of glutamic acid decarboxylase reduces neuropathic pain. Hao, S., Mata, M., Wolfe, D., Huang, S., Glorioso, J.C., Fink, D.J. Ann. Neurol. (2005) [Pubmed]
  5. Antiinflammatory and analgesic effects of somatostatin released from capsaicin-sensitive sensory nerve terminals in a Freund's adjuvant-induced chronic arthritis model in the rat. Helyes, Z., Szabó, A., Németh, J., Jakab, B., Pintér, E., Bánvölgyi, A., Kereskai, L., Kéri, G., Szolcsányi, J. Arthritis Rheum. (2004) [Pubmed]
  6. Altered visceral sensation in response to somatic pain in the rat. Miranda, A., Peles, S., Rudolph, C., Shaker, R., Sengupta, J.N. Gastroenterology (2004) [Pubmed]
  7. Effects of intrathecal strychnine and bicuculline on nerve compression-induced thermal hyperalgesia and selective antagonism by MK-801. Yamamoto, T., Yaksh, T.L. Pain (1993) [Pubmed]
  8. Disappearance of morphine-induced hyperalgesia after discontinuing or substituting morphine with other opioid agonists. Sjøgren, P., Jensen, N.H., Jensen, T.S. Pain (1994) [Pubmed]
  9. Gabapentin antinociception in mice with acute herpetic pain induced by herpes simplex virus infection. Takasaki, I., Andoh, T., Nojima, H., Shiraki, K., Kuraishi, Y. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  10. The effect of chronic oral desipramine on capsaicin-induced allodynia and hyperalgesia: a double-blinded, placebo-controlled, crossover study. Wallace, M.S., Barger, D., Schulteis, G. Anesth. Analg. (2002) [Pubmed]
  11. Proteinase-activated receptor-2 and hyperalgesia: A novel pain pathway. Vergnolle, N., Bunnett, N.W., Sharkey, K.A., Brussee, V., Compton, S.J., Grady, E.F., Cirino, G., Gerard, N., Basbaum, A.I., Andrade-Gordon, P., Hollenberg, M.D., Wallace, J.L. Nat. Med. (2001) [Pubmed]
  12. Interleukin-1beta-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity. Samad, T.A., Moore, K.A., Sapirstein, A., Billet, S., Allchorne, A., Poole, S., Bonventre, J.V., Woolf, C.J. Nature (2001) [Pubmed]
  13. Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia. Davis, J.B., Gray, J., Gunthorpe, M.J., Hatcher, J.P., Davey, P.T., Overend, P., Harries, M.H., Latcham, J., Clapham, C., Atkinson, K., Hughes, S.A., Rance, K., Grau, E., Harper, A.J., Pugh, P.L., Rogers, D.C., Bingham, S., Randall, A., Sheardown, S.A. Nature (2000) [Pubmed]
  14. Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X3 receptors. Souslova, V., Cesare, P., Ding, Y., Akopian, A.N., Stanfa, L., Suzuki, R., Carpenter, K., Dickenson, A., Boyce, S., Hill, R., Nebenuis-Oosthuizen, D., Smith, A.J., Kidd, E.J., Wood, J.N. Nature (2000) [Pubmed]
  15. Nocistatin, a peptide that blocks nociceptin action in pain transmission. Okuda-Ashitaka, E., Minami, T., Tachibana, S., Yoshihara, Y., Nishiuchi, Y., Kimura, T., Ito, S. Nature (1998) [Pubmed]
  16. Noradrenaline hyperalgesia is mediated through interaction with sympathetic postganglionic neurone terminals rather than activation of primary afferent nociceptors. Levine, J.D., Taiwo, Y.O., Collins, S.D., Tam, J.K. Nature (1986) [Pubmed]
  17. Hyperalgesia mediated by spinal glutamate or substance P receptor blocked by spinal cyclooxygenase inhibition. Malmberg, A.B., Yaksh, T.L. Science (1992) [Pubmed]
  18. Effects of long-term corn consumption on brain serotonin and the response to electric shock. Lytle, L.D., Messing, R.B., Fisher, L., Phebus, L. Science (1975) [Pubmed]
  19. Bradykinin and inflammatory pain. Dray, A., Perkins, M. Trends Neurosci. (1993) [Pubmed]
  20. Spinal inflammatory hyperalgesia is mediated by prostaglandin E receptors of the EP2 subtype. Reinold, H., Ahmadi, S., Depner, U.B., Layh, B., Heindl, C., Hamza, M., Pahl, A., Brune, K., Narumiya, S., Müller, U., Zeilhofer, H.U. J. Clin. Invest. (2005) [Pubmed]
  21. Non-nociceptive environmental stress induces hyperalgesia, not analgesia, in pain and opioid-experienced rats. Rivat, C., Laboureyras, E., Laulin, J.P., Le Roy, C., Richebé, P., Simonnet, G. Neuropsychopharmacology (2007) [Pubmed]
  22. Dexamethasone prevents visceral hyperalgesia but not colonic permeability increase induced by luminal protease-activated receptor-2 agonist in rats. Róka, R., Ait-Belgnaoui, A., Salvador-Cartier, C., Garcia-Villar, R., Fioramonti, J., Eutamène, H., Bueno, L. Gut (2007) [Pubmed]
  23. Phosphorylation of transcription factor CREB in rat spinal cord after formalin-induced hyperalgesia: relationship to c-fos induction. Ji, R.R., Rupp, F. J. Neurosci. (1997) [Pubmed]
  24. Hypoactivity of the spinal cannabinoid system results in NMDA-dependent hyperalgesia. Richardson, J.D., Aanonsen, L., Hargreaves, K.M. J. Neurosci. (1998) [Pubmed]
  25. Neonatal capsaicin treatment attenuates spinal Fos activation and dynorphin gene expression following peripheral tissue inflammation and hyperalgesia. Hylden, J.L., Noguchi, K., Ruda, M.A. J. Neurosci. (1992) [Pubmed]
  26. Noxious thermal and chemical stimulation induce increases in 3H-phorbol 12,13-dibutyrate binding in spinal cord dorsal horn as well as persistent pain and hyperalgesia, which is reduced by inhibition of protein kinase C. Yashpal, K., Pitcher, G.M., Parent, A., Quirion, R., Coderre, T.J. J. Neurosci. (1995) [Pubmed]
  27. Primary afferent second messenger cascades interact with specific integrin subunits in producing inflammatory hyperalgesia. Dina, O.A., Hucho, T., Yeh, J., Malik-Hall, M., Reichling, D.B., Levine, J.D. Pain (2005) [Pubmed]
  28. Role of the sensory neuron cytoskeleton in second messenger signaling for inflammatory pain. Dina, O.A., McCarter, G.C., de Coupade, C., Levine, J.D. Neuron (2003) [Pubmed]
  29. TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury. Obata, K., Katsura, H., Mizushima, T., Yamanaka, H., Kobayashi, K., Dai, Y., Fukuoka, T., Tokunaga, A., Tominaga, M., Noguchi, K. J. Clin. Invest. (2005) [Pubmed]
  30. A role for spinal nitric oxide in mediating visceral hyperalgesia in the rat. Coutinho, S.V., Gebhart, G.F. Gastroenterology (1999) [Pubmed]
  31. Interleukin-1 beta as a potent hyperalgesic agent antagonized by a tripeptide analogue. Ferreira, S.H., Lorenzetti, B.B., Bristow, A.F., Poole, S. Nature (1988) [Pubmed]
  32. NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels. Zhang, X., Huang, J., McNaughton, P.A. EMBO J. (2005) [Pubmed]
  33. The NK1 receptor mediates both the hyperalgesia and the resistance to morphine in mice lacking noradrenaline. Jasmin, L., Tien, D., Weinshenker, D., Palmiter, R.D., Green, P.G., Janni, G., Ohara, P.T. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  34. Pharmacological analysis of cyclooxygenase-1 in inflammation. Smith, C.J., Zhang, Y., Koboldt, C.M., Muhammad, J., Zweifel, B.S., Shaffer, A., Talley, J.J., Masferrer, J.L., Seibert, K., Isakson, P.C. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  35. Substance P: does it produce analgesia or hyperalgesia? Oehme, P., Hilse, H., Morgenstern, E., Göres, E. Science (1980) [Pubmed]
  36. Hyperalgesic properties of 15-lipoxygenase products of arachidonic acid. Levine, J.D., Lam, D., Taiwo, Y.O., Donatoni, P., Goetzl, E.J. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  37. Prostaglandins inhibit endogenous pain control mechanisms by blocking transmission at spinal noradrenergic synapses. Taiwo, Y.O., Levine, J.D. J. Neurosci. (1988) [Pubmed]
  38. The effect of thalidomide treatment on vascular pathology and hyperalgesia caused by chronic constriction injury of rat nerve. Sommer, C., Marziniak, M., Myers, R.R. Pain (1998) [Pubmed]
  39. Central components of the analgesic/antihyperalgesic effect of nimesulide: studies in animal models of pain and hyperalgesia. Tassorelli, C., Greco, R., Sandrini, G., Nappi, G. Drugs (2003) [Pubmed]
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