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. 2021 Feb 28;22(5):2439. doi: 10.3390/ijms22052439

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Damage-associated molecular patterns (DAMPs) and pattern-recognition receptors (PRRs) changes at the acute phase of brain injury. (A) Morphological changes of neurons (grey), astrocytes (green), microglial and infiltrating leukocytes (blue), and DAMPs release (orange); (B) local field potential (LFP) and extracellular KCl recordings during the spreading depolarization triggered by the primary injury: the direct current (DC; 0–0.5Hz) shift is associated with a decrease of neuronal activity (AC; >0.5 Hz) and a KCl release; (C) Pattern-recognition receptors (PRRs) activation pathways; (D) kinetics of DAMPs and PRR expression as well as the course of cell death mechanisms. DAMPs: Damage-associated molecular patterns; IL: Interleukin; iNOS: inducible nitric oxide synthase; LFP: local field potential; MLKL: Mixed-lineage kinase domain-like pseudokinase; MyD88: Myeloid differentiation primary response 88; NFκB: nuclear factor-kappa B; RAGE: Receptor for advanced glycation end-products; RIPK1: receptor-interacting protein kinase 1; TLR: Toll-like receptor; TNF: Tumor necrosis factor; TNFR1: Tumor necrosis factor receptor 1.