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. 2020 Jan 14;40(6):939–954. doi: 10.1007/s10571-019-00784-3

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© The Author(s) 2020

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. 6 — Representative DBS/HFS scheme suggested mechanism. Six-OHDA induces inflammation within the GP by activating A1, which attracts microglia cells and increases cytokines. STN–DBS/HFS while only slightly changing the number of astrocytes attenuates the classical inflammatory A1 astrocyte subtype by inhibiting NF-κB activation and cytokine release. The less activated astrocytes decrease microglia attraction reflecting in the inhibition of local cytokine release leading to improvement of inflammation within the GP