| Project/Area Number |
06671672
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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 |
Obstetrics and gynecology
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| Research Institution | Yokohama City University School of Medicine |
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Principal Investigator |
UEMURA Tsuguo Yokohama City University School of Medicine, Department of Obstetrics and Gynecology Associate professor, 医学部, 助教授 (40046040)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Hajime Yokohama City University School of Medicine, Department of Obstetrics and Gyneco, 医学部, 助手 (30254212)
SHIRASU Kazuhiro Yokohama City University School of Medicine, Department of Obstetrics and Gyneco, 医学部, 講師 (60171047)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | GnRH neuron / membrane potential / Ca^<2+> mobilization / GnRH / noradrenaline / GnRH律動的分泌 / patch clamp / multiple unit activity / Ca イオン / multiple unit activiry |
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| Research Abstract |
Noradrenaline (NA) is one of the most important neurotransmitters involved in the regulation of gonadotropin-releasing hormone (GnRH) secretion. In this study, the effects of NA on GnRH secretion, intracellular Ca^<2+> concentrations ([Ca^<2+>]i), and membrane potentials were investigated in immortalized hypothalamic neurons (GT1-7) to determine the direct effects of NA on GnRH cells.
Cells were perfused in a plastic minicolumn, and GnRH concentrations of the effluents were measured. NA increased the release of GnRH in a dose-dependent manner. Cells were loaded with 4 muM Fura 2-AM,and the ratio of the intensities of fluorescent emission at 510 nm with excitation at 340 and 380 nm was calculated at 100-ms intervals. NA increased the [Ca2+]i responses of single GnRH cells dose-dependently. The NA-induced [Ca^<2+>]i increase was attenuated in the absence of extracellular calcium and was blocked by the b-adrenergic antagonist propranolol, but not by the a-adrenergic antagonist phentolamine. The cell membrane potential was recorded with a whole-cell patch clamp amplifier with glass-electrodes. NA induced membrane depolarization under current-clamp conditions. The depolarization was also inhibited by propranolol, but not by phentolamine.
The results show that NA directly affects the membrane potential of GT1-7 cells via b-adrenergic receptors and induces Ca^<2+> mobilization ; these effects stimulate GnRH secretion.
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