Cannabis use disorder: from neurobiology to treatment
Bernard Le Foll, Victor M. Tang, Sergio Rueda, Leanne V. Trick, Isabelle Boileau
Bernard Le Foll, Victor M. Tang, Sergio Rueda, Leanne V. Trick, Isabelle Boileau
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Review Series

Cannabis use disorder: from neurobiology to treatment

Abstract

Cannabis has been legalized for medical and recreational purposes in multiple countries. A large number of people are using cannabis and some will develop cannabis use disorder (CUD). There is a growing recognition that CUD requires specific interventions. This Review will cover this topic from a variety of perspectives, with a particular emphasis on neurobiological findings and innovative treatment approaches that are being pursued. We will first describe the epidemiology and burden of disease of CUD, including risk factors associated with CUD (both in terms of general risk and genetic risk variants). Neurobiological alterations identified in brain imaging studies will be presented. Several psychosocial interventions that are useful for the management of CUD, including motivational enhancement therapy, behavioral and cognitive therapy, and contingency management, will be covered. Although no pharmacological interventions are yet approved for CUD, we present the most promising pharmacological interventions being tested.

Authors

Bernard Le Foll, Victor M. Tang, Sergio Rueda, Leanne V. Trick, Isabelle Boileau

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Figure 1

Signaling by endogenous and exogenous cannabinoids modifies synaptic activity at multiple levels.

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Signaling by endogenous and exogenous cannabinoids modifies synaptic act...
(A) There are two known endocannabinoids, called anandamide (AEA) and 2-arachidonoylglycerol (2-AG). Cannabis contains exogenous cannabinoids, including Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD). (B) Endogenous cannabinoid release prevents overstimulation of neurons, modulates the release of various neurotransmitters such as GABA and glutamate, and has downstream effects, notably on dopaminergic transmission. The enzyme fatty acid amide hydrolase (FAAH) degrades anandamide. The enzyme MAGL regulates 2-AG. THC stimulates the cannabinoid system by binding to CB1 and CB2 receptors. Compared with signaling by endogenous cannabinoids (normal state), chronic cannabis use likely results in changes in various components of the endocannabinoid system (e.g., CB1 and FAAH).