Myelin, a multilayered membrane insulation wrapped around the axons, increases axonal conduction velocity at least by 50 fold. Myelination around the axon is thought to be crucial for information processing by changing the timing of neural firing patterns during development and learning. Additionally, Stimulating myelination as a result of impulse activity in axons could enable myelin to be regulated by environmental experience, which could contribute to information processing and learning in the brain. We have demonstrated that local translation of MBP mRNA in oligodendrocyte processes is initialized myelin formation at the site of connection between oligodendrocytes and axons depending on neural activity. These findings provide new insight into how myelination, and thus conduction velocity and function of neural circuits, can be regulated by nervous system activity. Then to consider how activity dependent myelination can be involved in information processing, we used myelin proteolipid protein 1 (PLP1) over expression mouse (PLP-tg). PLP1 is one of the major protein components of the myelin sheath and is thought to have important roles for myelin homeostasis. To understand the neural basis of the cognitive impairment caused by the reduction of the neural conduction velocity, we used two-month-old PLP-tg mice which have a slight reduction of conduction velocity and combined in vivo two photon microscopy with a motor learning task. GFP-based Calcium Calmodulin probe (G-CaMP) was induced by an adeno-associated virus (AAV) injection in layer 2/3 of the M1 cortex to enable detecting a difference in the firing pattern of neuronal activity with a lever pulling motor learning task. PLP-tg showed increased spontaneous activity in response to lever pulling motor movement compared with wild type littermates, which associates with a disruption in the timing of synaptic inputs and a performance of the motor learning task. We would like to suggest that reduced axonal conduction velocity results in reduced synchronous activation of neurons within learning circuits to result in impaired motor learning task.