Advertisement

Neuroscience Bulletin

, 24:166 | Cite as

Roles of TRESK, a novel two-pore domain K+ channel, in pain pathway and general anesthesia

Minireview

Abstract

TRESK is the most recently reported two-pore domain K+ channel, and different from other two-pore domain channels in gene, molecular structure, electrophysiological and pharmacological properties. Although the current knowledge of this potassium channel is inadequate, researches have demonstrated that TRESK is remarkablely linked to acute and chronic pain by activation of calcineurin. The fact that TRESK is sensitive to volatile anesthetics and localization in central nerve system implies that TRESK may play a very important role in the mechanism mediating general anesthesia. The further research of TRESK may contribute to explore the underlying mechanism of some pathological conditions and yield novel treatments for some diseases.

Keywords

TRESK two-pore domain K+ channels calcineurin dorsal root ganglion 

一种新发现的双孔钾通道-TRESK 在疼痛及全身麻醉中的作用 黄东越, 于布为, 范秋维

摘要

TRESK是最近新发现的一种双孔钾通道, 其在基因、分子结构、生理药理学特性方面不同于其他类别的双孔钾通道。本文总结了TRESK的研究现状, 并根据目前的研究资料推测TRESK有可能通过激活钙调神经磷酸酶参与了急性和慢性疼痛的发生, 是吸入性全身麻醉药的作用靶点, 有可能通过对钙调神经磷酸酶的激活影响记忆, 从而参与吸入性全身麻醉药的术后遗忘效应。对TRESK的深入研究有可能揭示某些病理生理状态的内在机制。

关键词

TRESK 双孔钾通道 钙调神经磷酸酶 背根神经节 

CLC number

R33 

References

  1. [1]
    Ocaña M, Cendán CM, Cobos EJ, Entrena JM, Baeyens JM. Potassium channels and pain: present realities and future opportunities. Eur J Pharmacol 2004, 500: 203–219.PubMedCrossRefGoogle Scholar
  2. [2]
    Ketchum KA, Joiner WJ, Sellers AJ, Kaczmarek LK, Goldstein SA. A new family of outwardly rectifying potassium channel proteins with two pore domains in tandem. Nature 1995, 376: 690–695.PubMedCrossRefGoogle Scholar
  3. [3]
    Yost CS. Update on tandem pore (2P) domain K+ channels. Curr Drug Targets 2003, 4: 347–351.PubMedCrossRefGoogle Scholar
  4. [4]
    Lesage F, Lazdunski M. Molecular and functional properties of two-pore-domain potassium channels. Am J Physiol Renal Physiol 2000, 279: F793–F801.PubMedGoogle Scholar
  5. [5]
    Kim D. Physiology and pharmacology of two-pore domain potassium channels. Curr Pharm Des 2005, 11: 2717–2736.PubMedCrossRefGoogle Scholar
  6. [6]
    Goldstein SA, Bockenhauer D, O’Kelly I, Zilberberg N. Potassium leak channels and the KCNK family of two-P-domain subunits. Nat Rev Neurosci 2001, 2: 175–184.PubMedCrossRefGoogle Scholar
  7. [7]
    Sano Y, Inamura K, Miyake A, Mochizuki S, Kitada C, Yokoi H, et al. A novel two-pore domain K+ channel, TRESK, is localized in the spinal cord. J Biol Chem 2003, 278: 27406–27412.PubMedCrossRefGoogle Scholar
  8. [8]
    Kang D, Mariash E, Kim D. functional expression of TRESK-2, a new member of the tandem-pore K+ channel family. J Biol Chem 2004, 279: 28063–28070.PubMedCrossRefGoogle Scholar
  9. [9]
    Kang D, Kim D. TREK-2 (K2P 10.1) and TRESK (K2P 18.1) are major background K+ channels in dorsal root ganglion neurons. Am J Physiol Cell Physiol 2006, 291: C138–C146.PubMedCrossRefGoogle Scholar
  10. [10]
    Liu C, Au JD, Zou HL. Cotten JF, Yost CS. Potent activation of the human tandem pore domain K channel TRESK with clinical concentrations of volatile anesthetics. Anesth Analg 2004, 99: 1715–1722.PubMedCrossRefGoogle Scholar
  11. [11]
    Keshavaprasad B, Liu C, Au JD, Kindler CH, Cotten JF, Yost CS. species-specific differences in response to anesthetics and other modulators by the K2P channel TRESK. Anesth Analg 2005, 101: 1042–1049.PubMedCrossRefGoogle Scholar
  12. [12]
    Kandel ER, Schwartz JH, Jessell TM. Essentials of Neural Science and Behavior. Beijing: Science Pr., 2003, 173–177.Google Scholar
  13. [13]
    Czirják G, Enyedi P. Zinc and mercuric ions distinguish TRESK from the other two-pore-domain K+ channels. Mol Pharmacol 2006, 69: 1024–1032.PubMedGoogle Scholar
  14. [14]
    Devor M. Potassium channels moderate ectopic excitability of nerve-end neuromas in rats. Neurosci Lett 1983, 40:181–186.PubMedCrossRefGoogle Scholar
  15. [15]
    Dobler T, Springauf A, Tovornik S, Weber M, Schmitt A, Sedlmeier R, et al. TRESK two-pore-domain K+ channels constitute a significant component of background potassium currents in murine dorsal root ganglion neurones. J Physiol 2007, 585: 867–879.PubMedCrossRefGoogle Scholar
  16. [16]
    Czirják G, Toth ZE, Enyedi P. The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin. J Biol Chem 2004, 279: 18550–18558.PubMedCrossRefGoogle Scholar
  17. [17]
    Chung JM, Chung K. Importance of hyperexcitability of DRG neurons in neuropathic pain. Pain Pract 2002, 2: 87–97.PubMedCrossRefGoogle Scholar
  18. [18]
    Song XJ, Vizcarra C, Xu DS, Rupert RL, Wong ZN. Hyperalgesia and neural excitability following injuries to central and peripheral branches of axons and somata of dorsal root ganglion neurons. J Neurophysiol 2003, 89: 2185–2193.PubMedCrossRefGoogle Scholar
  19. [19]
    Wen YR, Suter MR, Kawasaki Y, Huang J, Pertin M, Kohno T, et al. Nerve conduction blockade in the sciatic nerve prevents but does not reverse the activation of p38 mitogen-activated protein kinase in spinal microglia in the rat spared nerve injury model. Anesthesiology 2007, 107: 312–321.PubMedCrossRefGoogle Scholar
  20. [20]
    Guo W, Wang H, Watanabe M, Shimizu K, Zou S, LaGraize SC, et al. Glial-cytokine-neuronal interactions underlying the mechanisms of persistent pain. J Neurosci 2007, 27: 6006–6018.PubMedCrossRefGoogle Scholar
  21. [21]
    Tsuda M, Mizokoshi A, Shigemoto-Mogami Y, Koizumi S, Inoue K. Activation of p38 mitogen-activated protein kinase in spinal hyperactive microglia contributes to pain hypersensitivity following peripheral nerve injury. Glia 2004, 45: 89–95.PubMedCrossRefGoogle Scholar
  22. [22]
    Ji RR, Suter MR. p38 MAPK, microglial signaling, and neuropathic pain. Mol Pain 2007, 3: 33.PubMedCrossRefGoogle Scholar
  23. [23]
    Zhuang ZY, Kawasaki Y, Tan PH, Wen YR, Huang J, Ji RR. Role of the CX3CR1/p38 MAPK pathway in spinal microglia for the development of neuropathic pain following nerve injury-induced cleavage of fractalkine. Brain Behav Immun 2007, 21: 642–651.PubMedCrossRefGoogle Scholar
  24. [24]
    Ji RR, Woolf CJ. Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain. Neurobiol Dis 2001, 8: 1–10.PubMedCrossRefGoogle Scholar
  25. [25]
    Vadivelu N, Sinatra R. Recent advances in elucidating pain mechanisms. Curr Opin Anaesthesiol 2005, 18: 540–547.PubMedCrossRefGoogle Scholar
  26. [26]
    Smith HS. Arachidonic acid pathways in nociception. J Support Oncol 2006, 4: 277–287.PubMedGoogle Scholar
  27. [27]
    Woo YC, Park SS, Subieta AR, Brennan TJ. Changes in tissue, pH and temperature after incision indicate acidosis may contribute to postoperative pain. Anesthesiology 2004, 101: 468–475.PubMedCrossRefGoogle Scholar
  28. [28]
    Czirjak G, Enyedi P. Targeting of calcineurin to an NFAT-like docking site is required for the calcium-dependent activation of the background K+ channel, TRESK. J Biol Chem 2006, 281: 14677–14682.PubMedCrossRefGoogle Scholar
  29. [29]
    Mansuy IM. Calcineurin in memory and bidirectional plasticity. Biochem Biophys Res Commun 2003, 311: 1195–1208.PubMedCrossRefGoogle Scholar
  30. [30]
    Groth RD, Dunbar RL. Mermelstein PG.Calcineurin regulation of neuronal plasticity. Biochem Biophys Res Commun 2003, 311: 1159–71PubMedCrossRefGoogle Scholar
  31. [31]
    Noda Y, Kodama K, Yasuda T, Takahashi S. Calcineurin-inhibitor-induced pain syndrome after bone marrow transplantation. J Anesth 2008, 22: 61–63.PubMedCrossRefGoogle Scholar
  32. [32]
    Goffin EJ. Calcineurin-inhibitors and bone pain after organ transplantation. Kidney Int 2007, 71: 468.PubMedCrossRefGoogle Scholar
  33. [33]
    Takashima S, Numata A, Miyamoto T, Shirakawa T, Kinoshita R, Kato K, et al. Acute lymphoblastic leukemia presenting with calcineurin-inhibitor induced pain syndrome after a second allogeneic bone marrow transplantation. Rinsho Ketsueki 2006, 47: 1372–1376.PubMedGoogle Scholar
  34. [34]
    Fujii N, Ikeda K, Koyama M, Aoyama K, Masunari T, Kondo E, et al. Calcineurin inhibitor-induced irreversible neuropathic pain after allogeneic hematopoietic stem cell transplantation. Int J Hematol 2006, 83: 459–461.PubMedCrossRefGoogle Scholar
  35. [35]
    Kida A, Ohashi K, Tanaka C, Kamata N, Akiyama H, Sakamaki H. Calcineurin-inhibitor pain syndrome following haematopoietic stem cell transplantation. Br J Haematol 2004, 126: 288.PubMedCrossRefGoogle Scholar
  36. [36]
    Luo J, Yin JH, Wu HZ, Wei Q. Extract from Fructus cannabis activating calcineurin improved learning and memory in mice with chemical drug-induced dysmnesia. Acta Pharmacol Sin 2003, 24: 1137–1142.PubMedGoogle Scholar
  37. [37]
    Clarkson AN. Anesthetic-mediated protection/preconditioning during cerebral ischemia. Life Sci 2007, 80: 1157–1175.PubMedCrossRefGoogle Scholar
  38. [38]
    Ozer M, Baris S, Karakaya D, Kocamanoglu S, Tur A. Behavioural effects of chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane in rats. Can J Anaesth 2006, 53: 653–658.PubMedCrossRefGoogle Scholar
  39. [39]
    Yu DY, Luo J, Bu F, Song GJ, Zhang LQ, Wei Q. Inhibition of calcineurin by infusion of CsA causes hyperphosphorylation of tau and is accompanied by abnormal behavior in mice. Biol Chem 2006, 387: 977–983.PubMedCrossRefGoogle Scholar

Copyright information

© Shanghai Institutes for Biological Sciences, CAS and Springer-Verlag GmbH 2008

Authors and Affiliations

  1. 1.Department of AnesthesiologyRuijin Hospital, Shanghai Jiao Tong University School of MedicineShanghaiChina

Personalised recommendations