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. 2021 Nov 12;38(6):927–943. doi: 10.1007/s10565-021-09677-y

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© The Author(s) 2021

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. 4 — Sevoflurane regulated signaling pathways through AMPAR and NMDAR, which result in abnormal synaptic plasticity. HDAC6, P25/CDK5/GSK-3β axis, P25/CDK5/CRMP2 axis, and ubiquitination-proteasome involved in these signaling pathways, which activation could decrease PSD-95, drebrin, and synaptophysin levels, resulting in synaptic plasticity decreased and cognitive impairment. Sevoflurane could decrease synaptic plasticity through CRH/CRHR1/Nectin-1axis, MeCP2/CREB/BNDF/SIRT1 axis, NR2B/Nova2/Netrin-1/DCC axis, and tPA/PAI-1/BNDF/TrkB axis, which induce synaptic plasticity decreased and cognitive impairment also. The dotted line bids for missing synapses