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. 2018 Apr 20;15:117. doi: 10.1186/s12974-018-1154-0

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Diagram of glial IL-1β-induced upregulation of neuronal Nav1.7 contributed to TMJ inflammatory hypernociception through the COX-2/PGE2/EP2-evoked PKA/CREB signaling pathway. TMJ inflammation somehow activates SGCs, which activate the transcriptions of IL-1β and COX-2 leading to increase in PGE2 release from the SGCs to subsequently activate the neuronal EP2/PKA/CREB signaling pathway then leading to upregulation of Nav1.7 in neurons and finally the increase in the neuronal excitability, which amplifies the stimuli in the TMJ contributing to the development of TMJ inflammatory hypernociception. TG, trigeminal ganglion; N, neuron; SGC, satellite glial cells