Effect of Repetitive Passive Movement Before Motor Skill Training on Corticospinal Excitability and Motor Learning Depend on BDNF Polymorphisms.

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A decrease in cortical excitability tends to be easily followed by an increase induced by external stimuli via a mechanism aimed at restoring it; this phenomenon is called “homeostatic plasticity.” In recent years, although intervention methods aimed at promoting motor learning using this phenomenon have been studied, an optimal intervention method has not been established. In the present study, we examined whether subsequent motor learning can be promoted further by a repetitive passive movement, which reduces the excitability of the primary motor cortex (M1) before motor learning tasks. We also examined the relationship between motor learning and the brain-derived neurotrophic factor. Forty healthy subjects (Val/Val genotype, 17 subjects; Met carrier genotype, 23 subjects) participated. Subjects were divided into two groups of 20 individuals each. The first group was assigned to perform the motor learning task after an intervention consisting in the passive adduction–abduction movement of the right index finger at 5 Hz for 10 min (RPM condition), while the second group was assigned to perform the task without the passive movement (control condition). The motor learning task consisted in the visual tracking of the right index finger. The results showed that the corticospinal excitability was transiently reduced after the passive movement in the RPM condition, whereas it was increased to the level detected in the control condition after the motor learning task. Furthermore, the motor learning ability was decreased immediately after the passive movement; however, the motor performance finally improved to the level observed in the control condition. In individuals carrying the Val/Val genotype, higher motor learning was also found to be related to the more remarkable changes in corticospinal excitability caused by the RPM condition. This study revealed that the implementation of a passive movement before a motor learning tasks did not affect M1 excitatory changes and motor learning efficiency; in contrast, in subjects carrying the Val/Val polymorphism, the more significant excitatory changes in the M1 induced by the passive movement and motor learning task led to the improvement of motor learning efficiency. Our results also suggest that homeostatic plasticity occurring in the M1 is involved in this improvement.