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. 2022 Sep 13;48(1):37–53. doi: 10.1038/s41386-022-01438-7

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© The Author(s), under exclusive licence to American College of Neuropsychopharmacology 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 1 — Schematic diagram of eCB signaling elements within synapses, astrocytes and microglia. At the synapse, eCBs are synthesized postsynaptically, through a variety of mechanisms that result in increases in intracellular calcium, and activate presynaptic CB1 receptors to mediate retrograde suppression of neurotransmitter release. AEA can also activate TRPV1 receptors to initiate postsynaptic LTD via glutamate receptor internalization. CB1 receptors expressed on astrocytes can lead to increases in calcium release and release of gliotransmitters, which can indirectly affect synaptic transmission. CB2 receptors on microglia can regulate cytokine release. CB1 receptors expressed on mitochondria can also regulate a variety of intracellular processes including cellular energetics.