| Project/Area Number |
62480242
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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 |
Psychiatric science
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
WATANABE Akiko (1988-1989) Tokyo Medical and Dental University,, 医学部・文部技官(教務職員) (40210992)
高橋 良 (1987) 東京医科歯科大学, 医学部, 教授 (70009918)
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| Co-Investigator(Kenkyū-buntansha) |
NANKAI Masahiro Tokyo Medical and Dental University, Teaching Staff., 医学部, 助手 (20218069)
KANENO Shigeru Tokyo Medical and Dental University, Teaching Staff., 医学部, 助手 (90126219)
仙波 純一 東京医科歯科大学, 医学部, 助手 (30183429)
渡辺 明子 東京医科歯大学, 医学部, 教務職員
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| Project Period (FY) |
1987 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | AFFECTIVE DISORDER / PARANOID SCHIZOPHRENIA / BETA-PHENYLETHYLAMINE / IMIPRAMINE BINDING / PAROXETINE BINDING / MONOAMINE OXIDASE / ヒト血小板 / ストレス / 双極感情病 / 5-HT取り込み / ^3H-imipramine結合 / ^3H-paroxetine結合 / うつ病血清 / 除タンパク血清 / 5ーHT取り込み / ^3Hーimipramine結合 / ^3Hーparoxetine結合 |
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| Research Abstract |
Urinary beta-phenylethylamine ( PEA ), one of biological markers in both affective disorder and paranoid schizophrenia, was examined in rapid cycler bipolar disorder. Increase in urinary PEA was found preceding the switch from mania to depression. This finding suggests that PEA plays the role of a biological trigger in the switch mechanism of a rapid cycler, especially in the switch from mania to depression. Secondary, we studied the role of PEA in schizophrenia. Schizophrenia was divided into two types : paranoid and non-paranoid. Increased urinary PEA excretion was found only in paranoid schizophrenia. A relationship between platelet monoamine oxidase (MAO) activity and urinary PEA excretion was found. These results suggest that PEA plays different roles in bipolar disorder and schizophrenia.
We previously reported the mean maximum number of binding sites (Bmax) of imipramine in depressed patients was significantly lower than that in healthy controls. A significant negative correlation was found between the Bmax values and total scores of the 17-item Hamilton depression rating scale in major depression, but not in bipolar disorder. In this study, we investigated platelet paroxetine binding in bipolar disorder. But, the Bmax of paroxetine binding was not significantly decreased compared to that of healthy controls. The hypothesis that endogenous inhibitors acting on imipramine binding sites was discussed. Then, we studied controls and depressed patients to conform whether the activity of endogenous inhibitors acting on imipramine binding. But inhibition activities of the imipramine and paroxetine by serum from controls and depressed patients were similar.
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