1989 Fiscal Year Final Research Report Summary
STUDIES ON THE MECHANISM OF ANTIDEPRESSANTS USING CLONAL CELL LINES (II)
| Project/Area Number |
63570511
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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 |
Psychiatric science
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| Research Institution | GUNMA UNIVERSITY (1989)
Saitama Medical University (1988) |
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Principal Investigator |
HIGUCHI Teruhiko GUNMA UNIVERSITY, FACULTY OF MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (90105883)
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| Co-Investigator(Kenkyū-buntansha) |
EBISAWA Takashi TOKYO METROPOLITAN INSTITUTE FOR NEUROSCIENCES, 分子神経生物学研究室, 流動研究員 (00201369)
MINATOGAWA Yukiko SAITAMA MEDICAL SCHOOL, INSTRUCTOR (60146272)
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| Project Period (FY) |
1988 – 1989
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| Keywords | Desipramine / beta-adrenergic receptors / Toxic effect / Intracellular accumulation / C_6 glioma cells / C_6グリオ-マ細胞 / 高速液体クロマトグラフィ- |
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| Research Abstract |
C_6 gliom cells were cultured in the medium containing desipramine(DMI) or haloperidol(HAL) for 4 days. Not only DMI but also HAL, in a dose of 10 muM, reduced the accumulation of cyclic AMP (cAMP) in the cells stimulated by isoproterenol. 10 muM DMI reduced both total cell protein and ATP level in the cells. Intracellular level of DMI was approximately 50-fold more concentrated than the extracellular level. It is likely that 10 muM of DMI in the medium induce toxic effect on C_6 cells due to the accumulation into the cells. Therefore, to investigate the mechanism of action of DMI using C_6 cells, its concentration in the medium should be less than 1 muM. Chronic exposure of C_6 cells to 0.1-1 muM DMI, in which doses neither total cell protein nor ATP level in the cells was affected, did not decrease cAMP accumulation.
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