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. 2018 Aug 1;8:11540. doi: 10.1038/s41598-018-29915-4

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Potential mechanism of EIH effects following VWR. (A) In NPP + Sedentary mice, pain perception activates RMTg/VTA-GABA neurons via activation of LHb-glutamatergic neurons. LDT neurons also activate VTA-GABA neurons. Activated RMTg/VTA-GABA neurons inhibit VTA-DA neurons, which may promote aversion, depression and reduction of ADL. These changes may function to maintain and deteriorate NPP. (B) In NPP + VWR mice, activation of lVTA-DA neurons via activation of both LDT-cholinergic/glutamatergic neurons and LHA-orexin neurons enhances DA release into the NAc, which may activate the mesolimbic reward system, and thereby produce EIH effects. Creation of positive emotion and pleasure following the attenuation of pain perception reinforces the motivation to perform physical exercise, further enhancing the EIH effects.