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. 2018 Aug 6;9:1047. doi: 10.3389/fphys.2018.01047

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Copyright © 2018 Larrieu and Layé.

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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PUFAs are key actors in the regulation of endocannabinoid system. Endocannabinoids are signaling lipids produced from membrane long-chain fatty acid in response to neuronal activity that bind the G-protein-coupled receptor (GPCR) CB1R. The two principal eCBs, AEA and 2-AG, are AA-derived metabolites while DHEA derived from the DHA. eCBs are released into the synaptic cleft and then bind the CB1R on the presynaptic neuron. Activation of CB1R inhibits adenylyl cyclase (AC) activity leading to a subsequent reduction in the cyclic adenosine monophosphate (cAMP) cascade, augmentation of potassium channels, and inhibition of subsequent calcium influx via calcium channels. Consequently, the activation of the CB1R inhibits the release of both excitatory (glutamate) and inhibitory (GABA) neurotransmitters from the presynaptic neuron and decreases synaptic plasticity. The stimulation of CB1R by CB agonists (THC, WIN55,212-2, and CP-55940) or eCBs also activate MAPK signaling pathway. Both eCB-dependent plasticity and CB1R-dependent signaling pathway in brain areas involved in mood-regulation are altered in mice that chronically fed an omega-3 deficient diet.