Fine motor control in rats is disrupted by delta-9-tetrahydrocannabinol

Evidence has suggested that cannabinoids such as THC, the active ingredient in marijuana, cause deficits in motor control and the production of movement. However, the specific components of motor control that are affected by cannabinoids have yet to be identified. The present study used an operant beam-press paradigm with a force criterion to determine the effects of THC on different parts of the force-time trajectory. Seven rats were trained to press a beam with at least 50 g of force to receive a sugar solution. THC was injected, as was apomorphine (APO), a selective dopamine D(2)/D(1) receptor agonist that acts as an antagonist at low doses. Low doses of APO, which have been found to cause deficits in motor execution, were used as a control for the effects of THC. Average peak force of a given press, as well as rate of rise of force, were significantly lowered by THC, as well as by apomorphine. Past research suggests that deficits in the rate of rise of force that can be attributed to depletions of dopamine in the nigrostriatal pathway, as in the case of low doses of APO, reflect failures of motor unit recruitment rather than of motor memory. Similarities in the motor effects of THC and APO suggest that THC plays a role in recruitment and synchronization of motor neurons appropriate for a given task.