Our ability to adapt to systematic perturbations makes it possible to maintain a lifetime of calibrated movements. Our focus here is on the neural basis of this motor memory. The current view is that adaptation depends critically on the cerebellum. However, over the last two years we, and others, have made a series of observations that challenge this view of adaptation. Here we suggest a different view of the problem of motor adaptation based on the core hypothesis that the cerebellum is embedded in a larger network that includes motor cortical areas, and that more than one mechanism is involved in forming a motor memory. Specifically, we suggest that motor memory is a result of interaction of distinct components: one component associates motor commands with sensory consequences, resulting in a forward model; one component searches the motor space for output that can produce a rewarding outcome, resulting in exploration; a third component relies on repetition to associate the sensory feedback with the motor commands, resulting in a feedback- dependent controller.
In Aim 1, we will test that idea that the function of M1 during adaptation is to encode a component of motor memory that depends on reinforced repetition of motor commands.
In Aim 2, we will test the hypothesis that damage to the cerebellum affects only one component of motor memory, the ability to form memories that depend on sensory prediction errors (forward models), but spares the ability to learn from repetition of motor commands. Our projects are clinically important because if we are right in that there are multiple neural pathways to formation of motor memory, then damage to one component may benefit from rehabilitation procedures that focus on remaining healthy neural structures. Our projects are important from a basic science standpoint because: (1) our experiments can connect the cerebellar-centric field of adaptation which has focused on error-dependent learning, with cerebral cortex-centric field of motor learning which has focused on repetition-dependent processes; (2) our experiments have the power to explain what is being 'prepared' by the brain during the preparatory period before movement onset; and finally (3) our experiments have the potential to actually test computational ideas that are very much in fashion in the field of optima control, and ask whether they have any relevance to the neural basis of motor control.
Cerebellar damage causes poor movement control and an inability to learn to improve movement. We will work to understand whether use of novel training schedules can improve motor learning. If so, we will ask whether this is because of involvement of other brain areas like the motor cortex. These approaches could be translated into novel and effective rehabilitation strategies.
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