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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. 6 — A, B WB revealed that O304 treatment abrogated the suppression effect of NTRK1 knockdown on the activity of the AMPK/ULK1/FUNDC1 pathway in mouse neurons. n = 3. C, D WB also indicated that O304 treatment counteracted the suppression effect of NTRK1 silencing on mitophagy in mouse neurons. n = 3. E, F The results of TOMM20/LC3-II fluorescence staining revealed that the O304 treatment reversed the suppression effect of NTRK1 knockdown on the expression of Parkin in mouse neuronmitochondria. n = 3. **P < 0.01.