|Budget Amount *help
¥114,920,000 (Direct Cost: ¥88,400,000、Indirect Cost: ¥26,520,000)
Fiscal Year 2011: ¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
Fiscal Year 2010: ¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
Fiscal Year 2009: ¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
Fiscal Year 2008: ¥21,970,000 (Direct Cost: ¥16,900,000、Indirect Cost: ¥5,070,000)
Fiscal Year 2007: ¥22,750,000 (Direct Cost: ¥17,500,000、Indirect Cost: ¥5,250,000)
In the adult mammalian central nervous system(CNS), it is well known that injured axons exhibit very limited regeneration ability. Due to this lack of appropriate axonal regeneration, a traumatic damage to the adult brain and spinal cord frequently causes permanent neuronal deficits such as paralysis. Several axon growth inhibitors in the CNS have been identified in the myelin. These proteins contribute to the lack of regeneration of the injured CNS. However, it is noted that spontaneous functional recovery sometimes occurs following CNS injury. Synaptic plasticity in pre-existing pathways and the formation of new circuits through collateral sprouting of lesioned and unlesioned fibers are important components of this spontaneous recovery process. Our research has focused on regeneration and plasticity of destructed neural network in the CNS. It unveiled the mechanism of plasticity of neural circuit after injury to the adult CNS, although it had been believed that adult CNS does not regenerate if damaged.