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. 2018 Oct 15;25(4):344–358. doi: 10.1177/1073858418805002

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© The Author(s) 2018

This article is distributed under the terms of the Creative Commons Attribution 4.0 License (http://www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — Possible mechanisms of seizure facilitation by interneurons. (A) Intense activity of interneurons during interictal bursts leads to GABA_A receptor–mediated Cl⁻ flux into principal neurons. This leads to KCC2-mediated efflux of K⁺ and Cl⁻. A seizure could then be triggered when extracellular K⁺ accumulation depolarizes a sufficient number of excitatory neurons. (B) When the capacity of principal neurons to extrude Cl⁻ is overwhelmed, Cl⁻ accumulation gradually shifts E_GABA to more depolarized potentials, weakening or even reversing the effect of GABA, and precipitating seizures. (C) Excessive activation of interneurons during interictal discharges causes them to enter a state of depolarization block. A seizure is generated when a sufficient number of interneurons cease firing and thus fail to contain excitatory activity.