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. 2023 Oct 31;9:404. doi: 10.1038/s41420-023-01685-7

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© The Author(s) 2023

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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Fig. 4 — A, B DCFH-DA staining results suggestedthatNTRK1 knockdown enhanced ROS accumulation in mouse neurons. n = 3. C The ATP content analysis indicated that NTRK1 knockdown resulted in reduced ATP content in mouse neurons. n = 3. D, E The results of JC-1 staining indicated thatNTRK1 knockdown decreased the mitochondrial membrane potential in mouse neurons. n = 3. F, G The mRFP-eGFP-LC3 assay revealed that NTRK1 knockdown suppressed the autophagic flux in mouse neurons. n = 3. **P < 0.01.