1992 Fiscal Year Final Research Report Summary
The molecular biological research for disorder of neuron and synaptic formation of the brain in congenital hydrocephalus
| Project/Area Number |
02454338
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Juntendo University School of Medicine |
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Principal Investigator |
SATO Kiyosi Juntendo University School of Medicine Department of Neurosurgery Professor & Chirman, 医学部, 教授 (10112707)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAJIMA Masakazu Juntendo University School of Medicine Department of Neurosurgery Assistant, 医学部, 助手 (60200177)
SUDA Kikuo Juntendo University School of Medicine Department of Neurosurgery Assistant, 医学部, 助手 (00206559)
TAKEDA Nobuaki Juntendo University School of Medicine Department of Neurosurgery Assistant, 医学部, 助手 (00171645)
ARAI Hajime Juntendo University School of Medicine Department of Neurosurgery Assistant Prof, 医学部, 講師 (70167229)
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| Project Period (FY) |
1990 – 1992
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| Keywords | Congenital Hydrocephalus / HTX-rats / Synapse Related Protein / Cytoskeletal Protein / Nerve Growth Factor |
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| Research Abstract |
In our experiments using congenitally hydrocephalic HTX-rats, we report some following matters concerned with disorder of neuron and synaptic formation of the brain.
1. Monoclonal antibodies against synaptic vesicle protein (SVP-38) and developmentally regulated brain proteins (Drebrins) were used to assess these two synapse related proteins by means of either a quantitative immunohistochemical method or a qualitative immunoblot analysis. The amount of SVP-38 decayed at 4 weeks after birth in hydrocephalic HTX-rats. When the hydrocephalic HTX-rats were treated with V-P shunt at 7 days after birth, such perturbations in postnatal changes of the SVP-38 were prevented completely. On the other hand postnatal decay of the embryonic form of Drebrins was considerably delayed in hydrocephalic HTX-rats. These observations suggest that synaptogenesis in the brain in the hydrocephalic HTX-rats is disturbed by the progression of hydrocephalus, and that early treatment of hydrocephalus may play a be
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neficial role not only in the repairing but also in the prevention of impaired synaptogenesis.
2. We investigated expressional and distributional changes of cytoskeletal proteins (tubulin, MAP-2 and tau protein) during developmental of brain in congenitally hydrocephalic HTX-rats using immunoblot analysis and immunohistochemical method. In the amount of and the distribution of tubulin and tau protein, there were no significant difference between non-hydrocephalic and hydrocephalic HTX-rats until 4 weeks of age. However, the amount of MAP-2, which is located in the dendrites of neurons, of 1 day old hydrocephalic rats have already decreased as compared with that of non-hydrocephalic rats at the same age. These observations seem to suggest that the metabolic disturbance of MAP-2 at the early developmental brain prevent the growth of dendrites of neurons and the maintenance of their final formation in the hydrocephalic brain.
3. Hydrocephalic associated changes in Choline Acetyltransferase (ChAT) activities and Nerve growth factor (NGF) in different areas (front-basal cortex, parieto-occipital cortex and hippocampus) of HTX-rat brains were determined. ChAT activity in the parieto-occipital cortex of 3 weeks old hydrocephalic rats was remarkable decreased, suggesting disturbance of the axonal transport of acetylcholine from the neurons in the basal forebrain to the parieto-occipital cortex. NGF concentration in the parieto-occipital cortex markedly increased with progression of hydrocephalus in comparison with that in the front-basal cortex and hippocampus. Such changes in regional increase of NGF may represent perturbation of neural mechanism in the developing brain affected by progressive hydrocephalus. Considering the experimental observations we have presented here, it would appear that one of the tasks required of pediatric neurosurgeons is the development of new surgical and medical treatment of congenital hydrocephalus in utero. Less
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