Project/Area Number |
21700382
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | Kumamoto University |
Principal Investigator |
SHINMYO Yohei Kumamoto University, 大学院・生命科学研究部, 助教 (00418831)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | Draxin / 反発活性 / 脳梁 / 視床皮質神経 / draxin / 反撥活性 |
Research Abstract |
In this study, we focused on Draxin functions in corpus callosum formation and thalamocortical projections. We found that Draxin has a critical role for the projections of corticothalamic and thalamocortical axons. Draxin is strongly expressed in early-born cortical neurons, including subplate and Cajal-Retzius cells, and weakly expressed in the ventral telencephalon and dorsal thalamus. Draxin deficient mice showed severe defects in the guidance of these axons : thalamocortical and corticothalamic axons followed an ectopic route through the external capsule instead of projecting to the cortex and thalamus, respectively. We found that thalamic axons showed a pathfinding error in the internal capsule region at embryonic day 14.5, when cortical axon pathfinding still appeared normal. This suggests that primary defects in the thalamocortical axon pathfinding cause misprojection of cortical axons. In addition, we showed that Draxin binds to thalamocortical axons and has inhibitory effects for neurite outgrowth from thalamic explants. Thus, we propose that Draxin repulsion from the neocortex may be essential for proper guidance of thalamocortical axons. We also found that Draxin repulsion is mediated by a receptor, dcc in the callosal neurons.
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