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Research ArticleNeuropharmacology

Inhibition of CaMKIIα in the Central Nucleus of Amygdala Attenuates Fentanyl-Induced Hyperalgesia in Rats

Zhen Li, Chenhong Li, Pingping Yin, Zaijie Jim Wang and Fang Luo
Journal of Pharmacology and Experimental Therapeutics October 2016, 359 (1) 82-89; DOI: https://doi.org/10.1124/jpet.116.233817
Zhen Li
Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Z.L., P.Y, F.L.); Laboratory of Membrane Ion Channels and Medicine, Key Laboratory of Cognitive Science, State Ethnic Affairs Commission, College of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China (C. L.); and Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, Illinois (Z.J.W)
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Chenhong Li
Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Z.L., P.Y, F.L.); Laboratory of Membrane Ion Channels and Medicine, Key Laboratory of Cognitive Science, State Ethnic Affairs Commission, College of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China (C. L.); and Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, Illinois (Z.J.W)
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Pingping Yin
Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Z.L., P.Y, F.L.); Laboratory of Membrane Ion Channels and Medicine, Key Laboratory of Cognitive Science, State Ethnic Affairs Commission, College of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China (C. L.); and Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, Illinois (Z.J.W)
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Zaijie Jim Wang
Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Z.L., P.Y, F.L.); Laboratory of Membrane Ion Channels and Medicine, Key Laboratory of Cognitive Science, State Ethnic Affairs Commission, College of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China (C. L.); and Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, Illinois (Z.J.W)
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Fang Luo
Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Z.L., P.Y, F.L.); Laboratory of Membrane Ion Channels and Medicine, Key Laboratory of Cognitive Science, State Ethnic Affairs Commission, College of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China (C. L.); and Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, Illinois (Z.J.W)
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Abstract

Opioid-induced hyperalgesia (OIH) is a less-studied phenomenon that has been reported in both preclinical and clinical studies. Although the underlying cause is not entirely understood, OIH is a real-life problem that affects millions of patients on a daily basis. Research has implicated the important contribution of Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) to OIH at the level of spinal nociceptors. To expand our understanding of the entire brain circuitry driving OIH, in this study we investigated the role of CaMKIIα in the laterocapcular division of the central amygdala (CeLC), the conjunctive point between the spinal cord and rostro-ventral medulla. OIH was produced by repeated fentanyl administration in the rat. Correlating with the development of mechanical allodynia and thermal hyperalgesia, CaMKIIα activity was significantly elevated in the CeLC in OIH. In addition, the frequency and amplitude of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in CeLC neurons were significantly increased in OIH. 2-[N-(2-hidroxyethyl)-N-(4-methoxy-benzenesulfonyl)]-amino-N-(4-chlorocinnamyl)-N-methylbenzylamine, a CaMKIIα inhibitor, dose dependently reversed sensory hypersensitivity, activation of CeLC CaMKIIα, and mEPSCs in OIH. Taken together, our data for the first time implicate a critical role of CeLC CaMKIIα in OIH.

Footnotes

    • Received March 23, 2016.
    • Accepted July 18, 2016.
  • ↵1 Z.L. and C.L. contributed equally to this work.

  • This work was supported by grants from the National Science Foundation of the People’s Republic of China [Grants 81328009, 81050023, and 81271234].

  • dx.doi.org/10.1124/jpet.116.233817.

  • Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 359 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 359, Issue 1
1 Oct 2016
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Research ArticleNeuropharmacology

CeLC CaMKIIα Contributes to Fentanyl-Induced Hyperalgesia

Zhen Li, Chenhong Li, Pingping Yin, Zaijie Jim Wang and Fang Luo
Journal of Pharmacology and Experimental Therapeutics October 1, 2016, 359 (1) 82-89; DOI: https://doi.org/10.1124/jpet.116.233817

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Research ArticleNeuropharmacology

CeLC CaMKIIα Contributes to Fentanyl-Induced Hyperalgesia

Zhen Li, Chenhong Li, Pingping Yin, Zaijie Jim Wang and Fang Luo
Journal of Pharmacology and Experimental Therapeutics October 1, 2016, 359 (1) 82-89; DOI: https://doi.org/10.1124/jpet.116.233817
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