β-arrestin-2-biased agonism of delta opioid receptors sensitizes transient receptor potential vanilloid type 1 (TRPV1) in primary sensory neurons

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• 作者：Matthew P Rowan ; Kalina Szteyn ; Allison P Doyle ; Ruben Gomez…
• 关键词：Chronic pain ; Opioid ; Allodynia ; Hyperalgesia
• 刊名：Molecular Pain
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：10
• 期：1
• 全文大小：1,134 KB
• 参考文献：1. Williams, JT, Ingram, SL, Henderson, G, Chavkin, C, von Zastrow, M, Schulz, S, Koch, T, Evans, CJ, Christie, MJ (2013) Regulation of mu-opioid receptors: desensitization, phosphorylation, internalization, and tolerance. Pharmacol Rev 65: pp. 223-254 CrossRef
  2. Angst, MS, Clark, JD (2006) Opioid-induced hyperalgesia: a qualitative systematic review. Anesthesiology 104: pp. 570-587 CrossRef
  3. Chen, Y, Yang, C, Wang, ZJ (2010) Ca2+/calmodulin-dependent protein kinase II alpha is required for the initiation and maintenance of opioid-induced hyperalgesia. J Neurosci 30: pp. 38-46 CrossRef
  4. Eijkelkamp, N, Wang, H, Garza-Carbajal, A, Willemen, HL, Zwartkruis, FJ, Wood, JN, Dantzer, R, Kelley, KW, Heijnen, CJ, Kavelaars, A (2010) Low nociceptor GRK2 prolongs prostaglandin E2 hyperalgesia via biased cAMP signaling to Epac/Rap1, protein kinase Cepsilon, and MEK/ERK. J Neurosci 30: pp. 12806-12815 CrossRef
  5. Elhabazi, K, Trigo, JM, Mollereau, C, Mouledous, L, Zajac, JM, Bihel, F, Schmitt, M, Bourguignon, JJ, Meziane, H, Petit-demouliere, B, Bockel, F, Maldonado, R, Simonin, F (2012) Involvement of neuropeptide FF receptors in neuroadaptive responses to acute and chronic opiate treatments. Br J Pharmacol 165: pp. 424-435 CrossRef
  6. Ferrini, F, Trang, T, Mattioli, TA, Laffray, S, Del’Guidice, T, Lorenzo, LE, Castonguay, A, Doyon, N, Zhang, W, Godin, AG, Mohr, D, Beggs, S, Vandal, K, Beaulieu, JM, Cahill, CM, Salter, MW, De Koninck, Y (2013) Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl(? homeostasis. Nat Neurosci 16: pp. 183-192 CrossRef
  7. Krishnan, S, Salter, A, Sullivan, T, Gentgall, M, White, J, Rolan, P (2012) Comparison of pain models to detect opioid-induced hyperalgesia. J Pain Res 5: pp. 99-106
  8. Li, X, Angst, MS, Clark, JD (2001) A murine model of opioid-induced hyperalgesia. Brain Res Mol Brain Res 86: pp. 56-62 CrossRef
  9. Lian, B, Vera-Portocarrero, L, King, T, Ossipov, MH, Porreca, F (2010) Opioid-induced latent sensitization in a model of non-inflammatory viscerosomatic hypersensitivity. Brain Res 1358: pp. 64-70 CrossRef
  10. Liang, DY, Liao, G, Wang, J, Usuka, J, Guo, Y, Peltz, G, Clark, JD (2006) A genetic analysis of opioid-induced hyperalgesia in mice. Anesthesiology 104: pp. 1054-1062 CrossRef
  11. Mao, J, Price, DD, Mayer, DJ (1994) Thermal hyperalgesia in association with the development of morphine tolerance in rats: roles of excitatory amino acid receptors and protein kinase C. J Neurosci 14: pp. 2301-2312
  12. Minville, V, Fourcade, O, Girolami, JP, Tack, I (2010) Opioid-induced hyperalgesia in a mice model of orthopaedic pain: preventive effect of ketamine. Br J Anaesth 104: pp. 231-238 CrossRef
  13. Vardanyan, A, Wang, R, Vanderah, TW, Ossipov, MH, Lai, J, Porreca, F, King, T (2009) TRPV1 receptor in expression of opioid-induced hyperalgesia. J Pain 10: pp. 243-252 CrossRef
  14. Zollner, C, Mousa, SA, Fischer, O, Rittner, HL, Shaqura, M, Brack, A, Shakibaei, M, Binder, W, Urban, F, Stein, C, Schafer, M (2008) Chronic morphine use does not induce peripheral tolerance in a rat model of inflammatory pain. J Clin Investig 118: pp. 1065-1073
  15. Chu, LF, Angst, MS, Clark, D (2008) Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations. Clin J Pain 24: pp. 479-496 CrossRef
  16. DuPen, A, Shen, D, Ersek, M (2007) Mechanisms of opioid-induced tolerance and hyperalgesia. Pain Manag Nurs 8: pp. 113
• 刊物主题：Pain Medicine; Molecular Medicine;
• 出版者：BioMed Central
• ISSN：1744-8069

文摘

Despite advances in understanding the signaling mechanisms involved in the development and maintenance of chronic pain, the pharmacologic treatment of chronic pain has seen little advancement. Agonists at the mu opioid receptor (MOPr) continue to be vital in the treatment of many forms of chronic pain, but side-effects limit their clinical utility and range from relatively mild, such as constipation, to major, such as addiction and dependence. Additionally, chronic activation of MOPr results in pain hypersensitivity known as opioid-induced hyperalgesia (OIH), and we have shown recently that recruitment of β-arrestin2 to MOPr, away from transient potential vanilloid eceptor type 1 (TRPV1) in primary sensory neurons contributes to this phenomenon. The delta opioid receptor (DOPr) has become a promising target for the treatment of chronic pain, but little is known about the effects of chronic activation of DOPr on nociceptor sensitivity and OIH. Here we report that chronic activation of DOPr by the DOPr-selective agonist, SNC80, results in the sensitization of TRPV1 and behavioral signs of OIH via β-arrestin2 recruitment to DOPr and away from TRPV1. Conversely, chronic treatment with ARM390, a DOPr-selective agonist that does not recruit β-arrestin2, neither sensitized TRPV1 nor produced OIH. Interestingly, the effect of SNC80 to sensitize TRPV1 is species-dependent, as rats developed OIH but mice did not. Taken together, the reported data identify a novel side-effect of chronic administration of β-arrestin2-biased DOPr agonists and highlight the importance of potential species-specific effects of DOPr agonists.