Motor habits are well learned spatiotemporally ordered sequences of movements executed without being explicitly motivated by a goal. Habits are formed following long trial-and-error learning periods but once acquired they tend to persist even when their beneficial outcome is degraded. Despite the behavioral importance of habits and their dramatic alteration in several pathologies (Parkinson disease, Tourette syndrome, addictions) the neuronal mechanisms behind habitual actions are unclear. On the one hand, lesions or dysfunction of the basal ganglia (BG) are well known to alter the formation and execution of habits. On the other hand, it is generally assumed that the function of the BG is to initiate adapted actions while inhibiting unwanted ones. This action selection model implies that the BG does not contribute to the control of the kinematics of actions (how selected actions are executed). A major problem of the action selection model is that it does not explain why BG dysfunctions result in specific deficits in movement kinematics.
Here, on the basis of recent findings from our team, we will test the hypothesis that, rather than selecting actions, neuronal activity in the BG plays a crucial role in controlling the kinematics of habitual actions. We will combine large-scale recordings of spiking activity in the BG (striatum) and related structures (primary motor cortex and thalamus) with optogenetic and pharmacological manipulations of neuronal activity in behaving rodents. Importantly we will use new behavioral tasks specifically designed to capture the often overlooked spatiotemporal structure of habits. The results obtained will shed new lights on the network and cellular mechanisms driving habits, the controversial function of the BG and the broader issue of motor learning. A better understanding of these topics is a required step toward improving the treatment of the numerous diseases of the BG, including those impairing habits.
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