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. 2018 Mar 5;8:3973. doi: 10.1038/s41598-018-22462-y

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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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Changes in synaptic plasticity of the corticostriatal pathway. (A) LTD was induced in the corticostriatal pathway in control animals (Open circle), while LTD was impaired in 6-OHDA lesioned animals (Open square). Partially recovered LTD could be found in the PD with exercise group, but this plasticity could not be maintained. (B) The input/output curve of the corticostriatal pathway, with significant enhancement of glutamatergic population spike in PD but a return to normal in the PD with exercise group under low stimulation intensity and increasing amplitude evoked by higher stimulation intensities. (C) The incidence (number) of synaptic plasticity formation in the corticostriatal pathway increased in exercise group compared with PD animals.