| Project/Area Number |
14572074
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
OKA Jun-ichiro Tokyo University of Science, Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (40134613)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Neurotrophic factor / GLP-1 / BDNF / Hippocampus / Motoneuron / Concussive brain injury / Learnina & memory / GLP-2 / 頭部外傷 / 神経損傷 / アスピリン / 炎症 / 神経突起伸長 / 神経生存率 / 初代培養 |
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| Research Abstract |
The final goal of the present study is to examine intracellular mechanisms of neurotrophic action of glucagon-like peptide-1(GLP-1)and its beneficial effects in brain diseases.First, we found that endogenous GLP-1 increased neurite length and branching of neurite without any effect on cell viability, indicating that it acts as a major neurotrophic factor in the brain of rat embryos in a manner similar to BDNF.Also we found that activation of cAMP and MAP kinase pathways may be involved in its effects.Second, we examined effects of exogenous GLP-1 and GLP-2 on brain dysfunction in model mice of the concussive brain injury.Our results demonstrated that GLP-1 or GLP-2 injected, icv.10 mm after the injury impaired memory impairment.Since aspirin but not indometacine injected s.c. alsof impaired memory impairment, inflammation may occur in the injured brain and, at least partially, cause memoryimpairment. G'LP-2 suppressed an increase in IL-1β.These results suggest that GLP-1 and GLP-2 have therapeutic effects on brain dysfunction induced with neuronal degeneration or brain injury.
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