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. 2020 Aug 7;11:3935. doi: 10.1038/s41467-020-17824-y

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© The Author(s) 2020

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. 9 — The diagram schematically illustrates the impact of ionic plasticity in SDH on laminar differences in synaptic plasticity. Higher activation of TrkB in LI, as compared to LII, which likely follows a gradient of BDNF availability from afferent fibers (green gradient and dots), sets a gradient in KCC2 expression increasing from dorsal to ventral (red gradient), leading to higher activity-dependent Cl⁻ accumulation in LI (blue gradient) and more robust inhibition in LII (yellow gradient). Higher ionic plasticity in LI results in a runaway, unconstrained plasticity, while it is more and more constrained in deeper laminae (purple gradient). The lamina-specific differences in synaptic plasticity affects modality-dependent sensitization induced by a dominant LI input (TRPV1 afferents, encoding thermal stimuli) or a dominant LII input (MRGPRD afferents, encoding mechanical stimuli).