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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. 1 — Effect of STN-DBS on apomorphine-induced rotational behavior and immobility induced by 6-OHDA. a In vivo experimental design. b Nissl staining analysis to confirm electrode implantation in the STN. Representation of 6-OHDA-induced PD model in saline, 6-OHDA, and 6-OHDA + electrode OFF groups. c–e Immunohistochemistry for TH in the striatum showing 6-OHDA-induced dopaminergic degeneration in the SN. Images are representative of four independent experiments. f Apomorphine-induced rotational behavior was evaluated in order to confirm the dopaminergic deficit. Values represent the mean + SEM (n = 4–8). *p < 0.05; **p < 0.001 vs. control saline group. g In vivo evaluation of immobility test following STN–DBS. Values represent the mean + SEM (n = 8 per group). ***p < 0.0001 vs. control saline group and $$$p < 0.0001 vs. 6-OHDA group. h Comparison between the immobility test performance before and after STN–DBS (immobility in the bar vs. before HFS in seconds) (n = 8 per group)