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. 2022 May 3;42:15. doi: 10.1186/s41232-022-00199-6

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Microglial modulation of neuroplasticity in the spinal dorsal horn and S1 that underlies chronic pain after PNS or CNS injury. TOP: the physical interaction and humoral factor release. BOTTOM: morphological and functional changes in microglia after PNS or CNS injury. Studies showing morphological changes in microglia have not shown specific functions, but have suggested their involvements in the pain development based on the molecular functions. Functional changes in microglia have been suggested to be factors released via TREM2/DAP12 or P2X4 signals. BDNF is one factor shown to be secreted from microglia in the spinal cord and brain after PNS or CNS injury, involved in pain development through synaptic remodeling and inducing hyperexcitability