1991 Fiscal Year Final Research Report Summary
Purification of ischemia induced neurotrophic factor and its application to the vascular dementia
| Project/Area Number |
02670628
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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 |
Cerebral neurosurgery
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| Research Institution | Osaka University |
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Principal Investigator |
HAYAKAWA Toru Osaka University Neurosurgery Professor, 医学部, 教授 (20135700)
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| Co-Investigator(Kenkyū-buntansha) |
大槻 秀夫 大阪大学, 医学部, 助手
YAMADA Kazuo Osaka University Neurosurgery Assistant Professor, 医学部, 講師 (90150341)
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| Project Period (FY) |
1990 – 1991
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| Keywords | cerebral Ischemia / Neurotrophic Factor / Retrograde Degeneration / bFGF / BFGF Receptor / Thalamic Degeneration |
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| Research Abstract |
We have detected neurotrophic activity in the brain tissue adjacent to the infarction caused by occlusion of the rat middle cerebral artery. The activity was purified by gel filtration from the samples obtained from cortex and thalamus 12 days after ischemia. The neurotrophic activity was only detected in the periinfarcted cortex and the factor supported both cortical and thalamic neurons. The activity was detected in fractions'with molecular weights of 67k, 32k, 12.4k, and the activity was partly blocked by anti-bFGF antibody. Therefore, we injected recombinant BFGF to the cisterna magna of the rats with middle cerebral occlusion, and BFGF significantly prevented thalamic degeneration after cortical infarction. We then detected expression of BFGF and its receptor MRNA expression. The BFGF MRNA was expressed in neurons and astrocytes 3 days after ischemia but not detected one day after ischemia. Receptor of the BFGF however, detected one day after ischemia and it lasted 7 to 14 days after ischemia. The thalamic neurons, which goes to degeneration had no expression of BFGF or its receptors. The result suggest that cessation of BFGF supply to the thalamic neurons are most likely related to the retrograde degeneration of the thalamus after cortical infarction. Administration of BFGF therefore, prevented degeneration of the thalamic neurons.
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