Fast and slow motor-skill learning are mediated by distinct neural processes
When we learn a new motor skill, we experience rapid improvement in motor performance during the initial training period and slowly improve with further training across subsequent days. Researchers at Duke University Medical Center now report evidence that certain neural circuits in the brain exhibit significant modulations in neuronal activity and connectivity during motor-skill learning and that distinct processes may mediate the neuronal changes that accompany the initial, fast phase of motor-skill learning compared to the longer-lasting, slower phase.
Previous studies had revealed changes during motor-skill learning in neural activity and connectivity in several brain areas, namely motor cortex and dorsal striatum, but the nature and dynamics of the plastic changes in these brain structures during the different phases of motor learning remained unclear.
In the new work, researchers Rui Costa, Dana Cohen, and Miguel Nicolelis at Duke University recorded the simultaneous neuronal activity in primary motor cortex and dorsolateral striatum of mice during the different phases of motor-skill learning. Neuronal activity was monitored in the mice as they learned, over multiple sessions, to remain on a rotating rod whose speed steadily increased. The researchers observed that cortico-striatal neural circuits undergo substantial changes during motor learning and found that this plasticity differs between fast and slow motor-skill learning. In addition, they discovered that during the initial fast, "within-session" learning, similar plastic processes evolved in parallel in motor cortex and dorsal striatum, whereas during slow, "across-session" learning, the activity changes in motor cortex and striatum differed. Perhaps somewhat surprisingly, these changes seemed to develop in the absence of alterations in the overall firing rate of the neuronal population in each brain area. These results may open interesting avenues for investigating the motor deficits observed in mouse models of neurodegenerative disorders, such as Parkinson's and Huntington's diseases.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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