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. 2024 Jan 15;14:1328885. doi: 10.3389/fphar.2023.1328885

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Copyright © 2024 Schouten, Dalle, Mantini and Koppo.

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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Schematic representation of potential receptor-dependent and independent mechanisms via which cannabidiol (CBD) may play a role in the treatment of therapeutic applications. The direct (ant)agonistic actions of CBD are depicted with arrows and lines toward the respective receptors. Additionally, the indirect receptor mechanisms of CBD, i.e., via increased anandamide (AEA) concentration [by inhibiting its hydrolysis to arachidonic acid via fatty acid amide hydrolase (FAAH)], and increased extracellular adenosine concentration [by inhibiting its uptake via equilibrative nucleoside transporter (ENT)] are included. The light grey inhibitory arrow indicates an antagonistic effect of CBD towards cannabinoid receptor 1 (CB1). However, it should be noted that CBD displays a low affinity for CB1 and a minimal direct activity at CB1. CB2: cannabinoid receptor 2; TRPV1: transient receptor potential vanilloid channel 1; TRPV2: transient receptor potential vanilloid channel 2; TRPA1: transient receptor potential ankyrin channel 1; TRPM8: transient receptor potential melastin channel 8; GABA_A: γ-aminobutyric acid type A receptor; PPARγ: peroxisome proliferator-activated receptor gamma; GPR55: G protein-coupled receptor 55; 5-HT1A: serotonin 1A receptor.