| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Research Abstract |
We have proposed that a fibrotic scar containing type IV collagen (Col IV) which is formed in the process of tissue repair after CNS injury acts as an impediment for axonal regeneration. This idea is based upon the following findings. (1) In 7-day-old newborn mice in which transected nigrostriatal dopaminergic (DA) axons can regenerate, the fibrotic scar is not formed in the lesion site (Kawano, et. al., 2005). (2) Prevention of fibrotic scar formation by treatment with 2, 2'-dipyridyl (DPY), an inhibitor of Col IV synthesis, promotes regeneration of transected nigrostriatal DA axons (Kawano, et. al., 2005).
In the present studies, (3) the fibrotic scar is not formed after injury of the hypothalamic arcuate nucleus, which promotes axonal regeneration of transected NPY neurons (Homma, et. al., 2006) (4) The fibrotic scar is eliminated in mice subjected to chondroitinase ABC (ChABC) treatment which degraded glycochains of CSPGs, suggesting that the promoting effect of ChABC on axonal regeneration is mediated via the elimination of fibrotic scar (Li, et. al., 2007).
In these all cases, the axonal regeneration occurs when the fibrotic scar is not formed, which strongly suggests that the fibrotic scar is a major impediment for axonal regeneration after CNS injury.
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