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. 2019 Jan 24;12:1053. doi: 10.3389/fnins.2018.01053

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Copyright © 2019 Gerace, Landucci, Bani, Moroni, Mannaioni and Pellegrini-Giampietro.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothetical model to explain mechanisms underlying ethanol withdrawal toxicity. Ethanol withdrawal potentiates the excitatory synaptic transmission that lead to CA1 injury of hippocampus in vitro. These alterations are probability due to the increase of the expression of the glutamate receptors AMPA (specifically the GluA1 AMPA subunit) and mGluR5. These evidences suggest that after ethanol withdrawal there is a shift in AMPAR subunit composition with the insertion of calcium permeable AMPA receptors in organotypic hippocampal slices.