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The literature suggests that direct agonism of A1/A2 receptors by CBD is unlikely due to its concentrationeffect (E/c) curve and surplus agonist concentration, and, as such, indirect elevation of local adenosine levels is not only more plausible, but could represent a viable mechanism underlying CBDs actions through those receptors [73,77,78,79]

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A long noncoding RNA contributes to neuropathic pain by silencing Kcna2 in primary afferent neurons