Publication Cover
Neurological Research
A Journal of Progress in Neurosurgery, Neurology and Neurosciences
Volume 43, 2021 - Issue 7
263
Views
8
CrossRef citations to date
0
Altmetric
Original Research Paper

Blockade of Spinal EphA4 Reduces Chronic Inflammatory Pain in Mice

, , &
Pages 528-534 | Received 28 Sep 2020, Accepted 28 Jan 2021, Published online: 04 Feb 2021

References

  • Kullander K, Klein R. Mechanisms and functions of Eph and ephrin signalling. Nat Rev Mol Cell Biol. 2002;3(7):475–486.
  • Xia WS, Peng YN, Tang LH, et al. Spinal ephrinB/EphBsignalling contributed to remifentanil-induced hyperalgesia via NMDA receptor. Eur J Pain. 2014;18(9):1231–1239.
  • Song XJ, Zheng JH, Cao JL, et al. EphrinB-EphB receptor signaling contributes to neuropathic pain by regulating neural excitability and spinal synaptic plasticity in rats. Pain. 2008;139(1):168–180.
  • Liu S, Liu WT, Liu YP, et al. Blocking EphB1 receptor forward signaling in spinal cord relieves bone cancer pain and rescues analgesic effect of morphine treatment in rodents. Cancer Res. 2011;71(13):4392–4402.
  • Slack S, Battaglia A, Cibert-Goton V, et al. EphrinB2 induces tyrosine phosphorylation of NR2B via Src-family kinases during inflammatory hyperalgesia. Neuroscience. 2008;156(1):175–183.
  • Filosa A, Paixao S, Honsek SD, et al. Neuron-glia communication via EphA4/ephrin-A3 modulates LTP through glial glutamate transport. Nat Neurosci. 2009;12(10):1285–1292.
  • Murai KK, Nguyen LN, Irie F, et al. Control of hippocampal dendritic spine morphology through ephrin-A3/EphA4 signaling. Nat Neurosci. 2003;6(2):153–160.
  • Ji RR, Kohno T, Moore KA, et al. Central sensitization and LTP: do pain and memory share similar mechanisms? Trends Neurosci. 2003;26(12):696–705.
  • Hylden JL, Wilcox JL. Intrathecal morphine in mice: a new technique. Eur J Pharmacol. 1980;67(2–3):313–316.
  • Billiau A, Matthys P. Modes of action of freund’s adjuvants in experimental models of autoimmune diseases. J Leukocyte Biol. 2001;70(6):849–860.
  • Hargreaves K, Dubner R, Brown F, et al. A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain. 1988;32(1):77–88.
  • Villarreal CF, Funez MI, Figueiredo F, et al. Acute and persistent nociceptive paw sensitisation in mice: the involvement of distinct signalling pathways. Life Sci. 2009;85(23–26):822–829.
  • Chaplan SR, Bach FW, Pogrel JW, et al. Quantitative assessment of tactile allodynia in the rat paw. J Neurosci Methods. 1994;53(1):55–63.
  • Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–254.
  • Coggeshall RE. Fos, nociception and the dorsal horn. Prog Neurobiol. 2005;77(5):299–352.
  • Munglani R, Fleming BG, Hunt SP. Remembrance of times past: the significance of c-Fos in pain. Br J Anaesth. 1996;76(1):1–4.
  • Coulthard MG, Morgan M, Woodruff TM, et al. Eph/Ephrin signaling in injury and inflammation. Am J Pathol. 2012;181(5):1493–1503.
  • Hruska M, Dalva MB. Ephrin regulation of synapse formation, function and plasticity. Mol Cell Neurosci. 2012;50(1):35–44.
  • Dong Y, Mao-Ying QL, Chen JW, et al. Involvement of EphB1 receptor/ephrinB1 ligand in bone cancer pain. Neurosci Lett. 2011;496(3):163–167.
  • Ruan JP, Zhang HX, Lu XF, et al. EphrinBs/EphBs signaling is involved in modulation of spinal nociceptive processing through a mitogen-activated protein kinases-dependent mechanism. Anesthesiology. 2010;112(5):1234–1249.
  • Zhou XL, Wang Y, Zhang CJ, et al. COX-2 is required for the modulation of spinal nociceptive information related to ephrinB/EphBsignalling. Eur J Pain. 2015;19(9):1277–1287.
  • Zhao J, Yuan G, Cendan CM, et al. Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain. Mol Pain. 2010;6:1744–8069–1746–1777.
  • Peng Y, Zang T, Zhou L, et al. COX-2 contributed to the remifentanil-induced hyperalgesia related to ephrinB/EphB signaling. Neurol Res. 2019;41(6):519–527.
  • Kania A, Klein R. Mechanisms of ephrin–Eph signalling in development, physiology and disease. Nat Rev Mol Cell Biol. 2016;17(4):240–256.
  • Klein R. Eph/ephrin signaling in morphogenesis, neural development and plasticity. Curr Opin Cell Biol. 2004;16(5):580–589.
  • Irizarry-Ramirez M, Willson CA, Cruz-Orengo L, et al. Upregulation of EphA3 receptor after spinal cord injury. J Neurotrauma. 2005;22(8):929–935.
  • Li YY, McTiernan CF, Feldman AM. IL-1 beta alters the expression of the receptor tyrosine kinase gene r-EphA3 in neonatal rat cardiomyocytes. Am J Physiol. 1998;274(1):H331–H341.
  • Kowalski EA, Chen J, Hazy A, et al. Peripheral loss of EphA4 ameliorates TBI-induced neuroinflammation and tissue damage. J Neuroinflammation. 2019;16(1):210–225.
  • Murai KK, Pasquale EB. Eph receptors and ephrins in neuron-astrocyte communication at synapses. Glia. 2011;59(11):1567–1578.
  • Munro KM, Dixon KJ, Gresle MM, et al. EphA4 receptor tyrosine kinase is a modulator of onset and disease severity of experimental autoimmune encephalomyelitis (EAE). PloS One. 2013;8(2):e55948.
  • Li J, Liu N, Wang Y, et al. Inhibition of EphA4 signaling after ischemia-reperfusion reduces apoptosis of CA1 pyramidal neurons. Neurosci Lett. 2012;518(2):92–95.
  • Goldshmit Y, Galea MP, Wise G, et al. Axonal regeneration and lack of astrocytic gliosis in EphA4-deficient mice. J Neurosci. 2004;24(45):10064–10073.
  • Cohen SP, Mao J. Neuropathic pain: mechanisms and their clinical implications. Bmj. 2014;348:f7656.
  • Kim MJ, Son JY, Ju JS, et al. Early blockade of EphA4 pathway reduces trigeminal neuropathic pain. J Pain Res. 2020;13:1173–1183.
  • Evdokimov D, Kreß L, Dinkel P, et al. Pain-associated mediators and axon pathfinders in fibromyalgia skin cells. J Rheumatol. 2020;47(1):140–148.
  • Vasileiou I, Adamakis I, Patsouris E, et al. Ephrinsand pain. Expert Opin Ther Targets. 2013;17(8):879–887.
  • Ji RR, Strichartz G. Cell signaling and the genesis of neuropathic pain. Sci STKE. 2004;2004(252):reE14.
  • Simonetti M, Hagenston Anna M, Vardeh D, et al. Nuclear calcium signaling in spinal neurons drives a genomic program required for persistent inflammatory pain. Neuron. 2013;77(1):43–57.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.