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. 2020 Aug 27;14:274. doi: 10.3389/fncel.2020.00274

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Copyright © 2020 Comer, Carrier, Tremblay and Cruz-Martín.

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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Neuroinflammation-induced dysfunctions that alter glutamatergic transmission in SCZ. Changes in glutamatergic transmission are known to occur in SCZ. Neuroinflammation impacts excitatory circuitry in SCZ through complement-mediated engulfment of excitatory synapses, the production of autoantibodies against NMDARs, changes in glutamate homeostasis potentially mediated by alterations in astrocytes and changes in the gut-brain axis, a known regulator of glutamate synthesis that is able to impact CNS functions such as stress responses. These changes in excitatory transmission can alter brain circuitry, for example, by altering synaptic plasticity and long-range excitation.