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. 2019 Mar 12;9:4165. doi: 10.1038/s41598-019-40729-w

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© The Author(s) 2019

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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Schematic of pathways associated with long-term potentiation in the pre-and post-synaptic membrane. Binding of Wnt5a to surface receptors on the pre-synaptic cell membrane (initiation of the Wnt signaling pathway) leads to mobilization of Ca2+ from intracellular stores (initiation of Ca2+ signaling pathway) and expression of N-methyl-D-aspartic acid receptors (NMDARs) on both pre-synaptic and postsynaptic membranes (initiation of the glutamatergic synapse pathway)³. Expression of NMDARs on the post-synaptic membrane facilitates the entry of Ca2+ which in turn activates calcium-calmodulin dependent protein kinase II (CaMKII) and mitogen-activated protein kinases (MAPKs) (initiation of the MAPK signaling pathway)³⁴. Together NMDARs and MAPK lead to phosphorylation and translocation of α-amino-3-hydrozy-5-methylisoxazole-4-propionic acid receptors (AMPARs) to the post synaptic membrane³⁶ where they increase synaptic conductance leading to long- term potentiation.