| Project/Area Number |
62571025
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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 |
応用薬理学・医療系薬学
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| Research Institution | Faculty of Medicine, Kyushu University |
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Principal Investigator |
KAZUMA Fujimoto Kyushu University, Faculty of Medicine, Assistant, 医学部, 助手 (50181392)
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| Co-Investigator(Kenkyū-buntansha) |
TOSHIIE Sakata Kyushu University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (50037420)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1987: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Histamine H_1-receptor / Hypothalamus / Ventromedial Hypothalamus / Paraventricular Nucleus / Feeding Behavior / Neuronal Histamine / αーfluoromethylhistidine / ヒスタミンH_1受容体拮抗薬 / 外側視床下野 / 視床下部背内側核 / 視索前野-前視床下野 / H_1受容体 / α-fluoromethylhistidine / ニューロン活動 |
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| Research Abstract |
To clarify the physiological role of hypotalamic histamine H_1-receptor in control of food intake, ingestive behavior and neuronal activities were investigated under blockade or diurnal flucturation of hypothalamic neuronal histamine. Histamine H_1-, but not H_2-receptor antagonists, potently induced feeding in a dose-related manner after infusion into rat third cerebroventricle in the light period. This feeding was elicited through ventromedial hypothlamus (VMH) and/or paraventricular neucleus (PVN). Elicitation was attenuated after infusion immediately before the dark when histamine content in the hypothalamus was low and abolished after intraperitoneal pretreatment with -fluoromethylhistidine (FMH), a specific suicide inhibitor of histidine decarboxylase. Electrophoretic application of a H_1-receptor antagonist to VMH neurons specifically suppressed activities of glucose-responding neurons. The suppressive effect was also attenuated by pretreatment with FMH. These results suggest that feeding induced by H_1-receptor antagonist is due to blokade of neuronal histamine at the site of histmaine H_1-receptors, at least in part, in VMH and PVN.
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