Abstract
Reinforcement and use-dependent plasticity mechanisms have been proposed to be involved in both savings and anterograde interference in adaptation to a visuomotor rotation (cf. Huang et al., 2011). In Parkinson's disease (PD), dopamine dysfunction is known to impair reinforcement mechanisms, and could also affect use-dependent plasticity. Here, we assessed savings and anterograde interference in PD with an A1-B-A2 paradigm in which movement repetition was (1) favored by the use of a single-target, and (2) manipulated through the amount of initial training. PD patients and controls completed either limited or extended training in A1 where they adapted movement to a 30° counter-clockwise rotation of visual feedback of the movement trajectory, and then adapted to a 30° clockwise rotation in B. After subsequent washout, participants readapted to the first 30° counter-clockwise rotation in A2. Controls showed significant anterograde interference from A1 to B only after extended training, and significant A1-B-A2 savings after both limited and extended training. However, despite similar A1 adaptation to controls, PD patients showed neither anterograde interference nor savings. That extended training was necessary in controls to elicit anterograde interference but not savings suggests that savings and anterograde interference do not result from equal contributions of the same underlying mechanism(s). It is suggested that use-dependent plasticity mechanisms contributes to anterograde interference but not to savings, while reinforcement mechanisms contribute to both. As both savings and anterograde interference were impaired in PD, dopamine dysfunction in PD might impair both reinforcement and use-dependent plasticity mechanisms during adaptation to a visuomotor rotation.
Highlights
Motor adaptation is the process through which the motor system alters movements to maintain performance in response to perturbations or changes in the state of the effector and/or of the environment
Parkinson’s disease (PD) patients did not show anterograde interference or savings after either limited or extended training in A1. These results indicate that different mechanisms contribute to savings and anterograde interference, and that these mechanisms are both impaired in PD
We suggest that the model-free mechanisms of reinforcement learning and use-dependent plasticity have different training requirements and show different contributions to anterograde interference and savings: while limited training might be sufficient to engage reinforcement mechanisms responsible for savings, extended www.frontiersin.org training might be necessary to engage other mechanisms to elicit anterograde interference
Summary
Motor adaptation is the process through which the motor system alters movements to maintain performance in response to perturbations or changes in the state of the effector and/or of the environment These perturbations evoke discrepancies between the predicted motor outcome and the actual motor outcome, which are thought to drive the iterative updating of an internal model that predicts the consequences of motor commands (i.e., a forward model; Thoroughman and Shadmehr, 1999). This internal-model based account of motor adaptation cannot fully explain persistent effects of initial learning on subsequent performance after the motor output is returned to the original, unadapted state (Huang et al, 2011). Two mechanisms have been suggested for this “model-free” slow process: reinforcement learning, where repeatedly pairing the adapted movement with a rewarding outcome (e.g., hitting the target) reinforces that movement such that there would be a subsequent bias toward reselecting that movement, and use-dependent plasticity, where repetition alone of a particular movement (i.e., independently of a reward associated with the adaptation) would bias subsequent movements toward the repeated movement (Huang et al, 2011)
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