2003 Fiscal Year Final Research Report Summary
Investigation for matching bHLH overexpressed transgenic mice to mood disorders model mice
| Project/Area Number |
13557079
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Psychiatric science
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| Research Institution | St Marianna University School of Medicine |
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Principal Investigator |
OSAKA Kenichi St. Marianna University School of Medicine, Department Neuropsychiatry, Associated Professor, 医学部, 講師 (20233504)
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| Co-Investigator(Kenkyū-buntansha) |
MATUI Kiroaki St. Mariaanna University School of Medicine, Radioisotope Research Institute, Professor, 医学部, 教授 (90181685)
ASAKURA Mikio St.Marianna University, School of Medicine, Department of Neuropsychiatry, Assistant Professor, 医学部, 助教授 (70103504)
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| Project Period (FY) |
2001 – 2003
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| Keywords | bHLH / Mod stabilizer / Lithium / GAP-43 / MATH / Transcription Factor / eEF2 / E-box |
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| Research Abstract |
Lithium is a mood stabilizer used in treatment of bipolar disorders. We reported that the GAP-43 RNA expression and GAP-43 protein levels 1.5 times increased after 4-5 weeks lithium treatment in the rat brain. GAP-43 is known to play an important role in the releasing process for several neurotransmitters (Ach, 5-HT and DA). We also reported that MATH-2 transcription factor bind the GAP-43 promoter ad increased in the expression for GAP-43.
MATH-2 increased the activity about 2.5 times compared with control in luciferase assay, and MATH-2 regulated GAP-43 gene expression than the other transcription factors. 5 week lithium treatment increased in the MATH-2 protein level about 4 times by immunoblot. Long-term lithium treatment translocated MATH-2 to nucleolus and nuclear membrane by immunohistochemistry.
We considered that MATH-2 induced increase of GAP-43 protein level and the long-term lithium treatment regulated GAP-43 by MATH-2.
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