Project/Area Number |
09307018
|
Research Category |
Grant-in-Aid for Scientific Research (A).
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Psychiatric science
|
Research Institution | Kagawa Medical University |
Principal Investigator |
SUWAKI Hiroshi Kagawa Medical University, Faculty of Medicine, Neuropsychiatry, Professor, 医学部, 教授 (10033367)
|
Co-Investigator(Kenkyū-buntansha) |
KURODA Shigetoshi Okayama University, Faculty of Medicine, Neuropsychiatry, Professor, 医学部, 教授 (00093683)
TAKEUCHI Yoshiki Kagawa Medical University, Faculty of Medicine, Anatomy, Professor, 医学部, 教授 (20116619)
MORIMOTO Kiyoshi Kagawa Medical University, Faculty of Medicine, Neuropsychiatry, Associate Professor, 医学部, 助教授 (20166432)
FUKUI Yoshihiro Tokushima University, Faculty of Medicine, Anatomy Professor, 医学部, 教授 (50144168)
TOKUNAGA Akira Okayama University, Faculty of Medicine, Anatomy, Professor, 医学部, 教授 (40009634)
岩橋 和彦 香川医科大学, 医学部・付属病院, 講師 (00232695)
|
Project Period (FY) |
1997 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥37,600,000 (Direct Cost: ¥37,600,000)
Fiscal Year 2000: ¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1999: ¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1998: ¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 1997: ¥17,300,000 (Direct Cost: ¥17,300,000)
|
Keywords | alcoholism / acetaldehyde adducts / hippocampus / calmodulin / FAS / antihypnotism / VTA / dopamine / 離脱症 / アポーシス / 逆耐性現象 / GABAAレセプター / アルコール / CaM-kinase / FAS / メタンフェタミン / GABA(A)レセプター / Syaptophysin / 分子遺伝学 / 大脳皮質 / 覚醒剤中毒 / 神経可塑性 / ドーパミン神経路 / 離脱 / モデル動物 / 免疫組織化学 / 大脳基底核 |
Research Abstract |
Acetaldehyde adduct seems to be a risk factor for brain damage in alcohol dependent and withdrawal animals. Furthermore, acetaldehyde adducts production and apoptosis-related gene expression in these animals were elucidated in the present study. On the other hand, abnormal formation of mossy fiber, LTP effects, strong expression of GluR2 subunit, editing of Q/R site and enzyme of CaM dependent phosphatase were observed in the hippocampus. With respect to peptides in the brain, expression of VIP-IR and DNA topoisomerase II β were apparently increased in the cerebral cortex and CA3 pyramidal cells, respectively. Calbindin D28k and GFAP-IR cells were found in the hippocampus and hypothalamus. It was of particularly interest that the expression of IR cells in the SCN of hypothalamus indicated the relationship with circadian rhythm. In FAS animals the ectopic cell mass in the cerebral cortex, abnormal distribution of mossy fibers, developmental anomaly of Purkinje and pyramidal cells and disappear of foot processes of Burgman glia cells were characteristically observed. In MAP dependent animals the neural plasticity was indicated to have relationship with arc gene, synaptophysin and α-tubulin. Additionally, the pathway of the midbrain VTA-Accumbence nucleus-Prefrontal cortex was also demonstrated to play an important role in abnormal behavior of the animals.
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