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Chronic use of cannabis might impair sensory error processing in the cerebellum through endocannabinoid dysregulation.

Adrián F Amil, Belén Rubio Ballester, Martina Maier, Paul Verschure

Addictive Behaviors August 2022 DOI: 10.1016/j.addbeh.2022.107297 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Cannabis
Keywords Cerebellum Chronic cannabis use Endocannabinoid system Error processing Motor learning
Key findings The authors propose that chronic cannabis use downregulates cerebellar CB1 receptors, leading to underestimation and misprocessing of sensory errors that normally drive synaptic updates in the cerebellar cortex. A computational model of motor adaptation reproduced the decreased implicit adaptation associated with chronic cannabis use, and the authors suggest this mechanism may also explain motor impairments following chronic alcohol dependence.

Abstract

Chronic use of cannabis leads to both motor deficits and the downregulation of CB1 receptors (CB1R) in the cerebellum. In turn, cerebellar damage is often related to impairments in motor learning and control. Further, a recent motor learning task that measures cerebellar-dependent adaptation has been shown to distinguish well between healthy subjects and chronic cannabis users. Thus, the deteriorating effects of chronic cannabis use in motor performance point to cerebellar adaptation as a key process to explain such deficits. We review the literature relating chronic cannabis use, the endocannabinoid system in the cerebellum, and different forms of cerebellar-dependent motor learning, to suggest that CB1R downregulation leads to a generalized underestimation and misprocessing of the sensory errors driving synaptic updates in the cerebellar cortex. Further, we test our hypothesis with a computational model performing a motor adaptation task and reproduce the behavioral effect of decreased implicit adaptation that appears to be a sign of chronic cannabis use. Finally, we discuss the potential of our hypothesis to explain similar phenomena related to motor impairments following chronic alcohol dependency.

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