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. 2017 Nov 15;7:15657. doi: 10.1038/s41598-017-16034-9

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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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Working model of resveratrol-induced modulation of IPSCs and I-LTD in the VTA. (a) In this model, PDEs degrade cAMP in VTA GABA neurons, leading to suppression of PKA activation of GABA release. GABA activates synaptic GABA_A receptors and perisynaptic GABA_B receptors to produce GABA_A- and GABA_B-IPSCs. Activation of the Gα_i/o-coupled CB₁ receptor also decreases cAMP/PKA signaling in presynaptic GABA axonal terminals, leading to I-LTD. (b) The non-selective PDE inhibitor resveratrol increases cAMP/PKA signaling by inhibiting cAMP degradation. As a result, GABA_A- and GABA_B-IPSCs are enhanced, and CB₁ receptor-mediated I-LTD is blocked. DA neuron means dopamine neuron.