1995 Fiscal Year Final Research Report Summary
Molecular mechanisms of defective cortical histogenesis in the cerebellar development.
| Project/Area Number |
06671171
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Okazaki National Research Institutes |
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Principal Investigator |
YUASA Shigeki Okazaki National Research Institutes, National Institute for Physiological Sciences, Department of Information Physiology, Associate Professor, 生理学研究所, 助教授 (70127596)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Tenascin / In situ hybridization / Radial glia / Reeler / Contact guidance / Neuronal migration / Cell adhesion molecule / Bergmann glia |
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| Research Abstract |
Neuron-glia interactions play important roles in the histogenesis of cortical structure during neural development, and the genetic disorders of such interactions may lead to the defective corticogenesis. In this study, neuron-glia interactions during cerebellar development were examined both in the normal and reeler mutant mice in order to elucidate the mechanisms of defective cortical formation. Expression of tenascin, a neuron-glia adhesion molecule, was used as the marker for embryonic radial glia and neonatal Bergmann glia in the developing cerebellum. Tenascin gene expression as examined by non-radioactive in situ hybridezation histochemistry revealed the mode of migration of the somata of radial glia, and tenascin-immunohistochemistry represented the dynamics of radial glial processes during cerebellar development. Radial glial somata migrated radially from the ventricular zone to the cortex and radial glial processes extending from ventricular zone to pia mater retracted towards the cortex after the contact guidance of Purkinje cell migration along tenascinimmunoreactive radial glial processes. These radial glia occupied a position corresponding to Bergmann glia in the postnatal cerebellum and showed GFAP-immunoreactivity along with the expression of tenascin gene. In the cerebellar development of the reeler cerebellum, the migration of Bergmann glial somata was obstructed in the pattern similar to subcortically situated Purkinje cells. The arrangement of both the processes and somata of Bergmann glia in the cortex was also defective. Only limited number of Bergmann glial processes were associated with Purkinje cells which were aligned in the cortex. These findings suggest that the defective cortical formation in the reeler cerebellum is due to the defect of Bergmann glial morphogenesis and the disorder of neuron-glia interactions during the contact guidance of Purkinje cell migration by radial glial processes.
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Research Products
(18 results)
