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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. 7 — A, B The results of NeuN IF staining revealed that rapamycin treatment counteracted the suppression effect of NTRK1 silencing on the expression of NeuN in mouse neurons. n = 3. C, D TUNEL staining indicated that rapamycin treatment reversed the promotion effect of NTRK1 silencing on the apoptosis of mouse neurons. n = 3. E The CCK-8 assay revealed that rapamycin treatment reversed the inhibition effect of silencing NTRK1 on the viability of mouse neurons. n = 3. F, G TOMM20/LC3-II fluorescence staining results revealed that rapamycin treatment abrogated the inhibition effect of NTRK1 silencing on the expression of Parkin1 in the mitochondria of mouse neurons. n = 3. H, I Mitochondria were extracted from the mouse neurons of each group. WB was performed, and it was revealed that rapamycin treatment reversed the suppression effect of NTRK1 silencing on mitophagy. n = 3. **P < 0.01.