Literature DB >> 30444263

Mitogen-activated protein kinase signaling mediates opioid-induced presynaptic NMDA receptor activation and analgesic tolerance.

Meichun Deng1,2, Shao-Rui Chen1, Hong Chen1, Yi Luo1,3, Yingchun Dong1,4, Hui-Lin Pan1.   

Abstract

Opioid-induced hyperalgesia and analgesic tolerance can lead to dose escalation and inadequate pain treatment with μ-opioid receptor agonists. Opioids cause tonic activation of glutamate NMDA receptors (NMDARs) at primary afferent terminals, increasing nociceptive input. However, the signaling mechanisms responsible for opioid-induced activation of pre-synaptic NMDARs in the spinal dorsal horn remain unclear. In this study, we determined the role of MAPK signaling in opioid-induced pre-synaptic NMDAR activation caused by chronic morphine administration. Whole-cell recordings of excitatory post-synaptic currents (EPSCs) were performed on dorsal horn neurons in rat spinal cord slices. Chronic morphine administration markedly increased the frequency of miniature EPSCs, increased the amplitude of monosynaptic EPSCs evoked from the dorsal root, and reduced the paired-pulse ratio of evoked EPSCs. These changes were fully reversed by an NMDAR antagonist and normalized by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2), p38, or c-Jun N-terminal kinase (JNK). Furthermore, intrathecal injection of a selective ERK1/2, p38, or JNK inhibitor blocked pain hypersensitivity induced by chronic morphine treatment. These inhibitors also similarly attenuated a reduction in morphine's analgesic effect in rats. In addition, co-immunoprecipitation assays revealed that NMDARs formed a protein complex with ERK1/2, p38, and JNK in the spinal cord and that chronic morphine treatment increased physical interactions of NMDARs with these three MAPKs. Our findings suggest that opioid-induced hyperalgesia and analgesic tolerance are mediated by tonic activation of pre-synaptic NMDARs via three functionally interrelated MAPKs at the spinal cord level. OPEN SCIENCE BADGES: This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at https://cos.io/our-services/open-science-badges/.
© 2018 International Society for Neurochemistry.

Entities:  

Keywords:  G protein-coupled receptor; NMDA receptor; opioid tolerance; primary afferent nerves; synaptic plasticity; μ-opioid receptor

Mesh:

Substances:

Year:  2018        PMID: 30444263      PMCID: PMC6340739          DOI: 10.1111/jnc.14628

Source DB:  PubMed          Journal:  J Neurochem        ISSN: 0022-3042            Impact factor:   5.372


  63 in total

1.  Opioid-induced long-term potentiation in the spinal cord is a presynaptic event.

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Authors:  K Fukuda; S Kato; H Morikawa; T Shoda; K Mori
Journal:  J Neurochem       Date:  1996-09       Impact factor: 5.372

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Authors:  D E Keith; S R Murray; P A Zaki; P C Chu; D V Lissin; L Kang; C J Evans; M von Zastrow
Journal:  J Biol Chem       Date:  1996-08-09       Impact factor: 5.157

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