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. 2017 Sep 11;7:11152. doi: 10.1038/s41598-017-11606-1

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© The Author(s) 2017

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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Schematic representation of CB1 receptor and FAAH in the dentate gyrus circuit: Both postsynaptic FAAH and presynaptic CB1 receptor are widely expressed and anatomically associated within the DG except for the PP-DG synapses and mossy fibers that do not express CB1 receptors. On the other hand, CB1 receptor is expressed in the excitatory mossy cell terminals projecting to granule cells and in the CA3 back-projecting terminals to granule cells. CB1 is also heavily expressed in the inhibitory GABAergic terminals, although the expression is restricted to a particular subpopulation of GABAergic interneurons (CCK⁺ interneurons)^36,38. During PPS (perforant path stimulation)-inducing either synaptic plasticity or MDA, these recurrent excitatory and inhibitory circuits are recruited and, a widespread non-selective activation of CB1 receptor within these circuits, such as after WIN administration, leads to an overall decrease of glutamate release which affects both MDA and synaptic plasticity occurrence. Conversely, AEA release is activity and regional dependent, and a fine tuning of GABA and glutamate transmissions depends on the spatio-temporal biosynthesis and release of AEA might occur in basal condition and during PPF-inducing synaptic plasticity which may further shift towards GABA inhibition when synaptic plasticity is induced in the epileptic circuit. When synaptic activation is strongly and persistently enhanced as during PPS-induced MDA, AEA effect may instead be prominent at glutamatergic synapses. Thus, inhibition of AEA degradation may increase the capability of the AEA to dampen excessive excitability without compromising its temporal and spatial specificity.