| Project/Area Number |
05454143
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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 |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KATAFUCHI Toshihiko Kyushu University, Dept.of Physiology, Associate Professor, 医学部, 講師 (80177401)
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| Co-Investigator(Kenkyū-buntansha) |
TAKE Sachiko Kyushu University, Dept.of Physiology, Assistant Professor, 医学部, 助手 (80253425)
TAKAKI Atsushi Kyushu University, Dept.of Physiology, Assistant Professor, 医学部, 助手 (30243934)
HORI Tetsuro Kyushu University, Dept.of Physiology, Professor, 医学部, 教授 (00022814)
粟生 修司 九州大学, 医学部, 助教授 (40150908)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1993: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | Splenic sympathetic nerve / interleukin-1beta / interferon-alpha / corticotropin-releasing factor / prostaglandin E2 / anterventral region of the III vetricle / glial cell / long term potentiation / EP1レセプター / c-fosタンパク / アンチセンスオリゴDNA / TNF / グルタミン酸 / 第3脳室壁前腹側領域 / CRF / 内側視索前野 / 視床下部室傍核 / ナチュラルキラー細胞活性 / スライスパッチ法 / NMDA応答電流 / 視床下部視索前野 / インターロイキンIL-1beta / 血液-脳関門 / インターフェロンalpha / ナチュラルキラー(NK)細胞 |
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| Research Abstract |
What we found by this project is as follows.
(1) Suppression of splenic natural killer (NK) cell activity by noradrenaline released from splenic sympathetic nerve (SSN) terminals is one of the mechanisms of immobilization-induced immunosuppression. (2) Brain IL-1beta induces reduction of cellular immunity at least partly through an activation of the SSN.(3) Immunosuppression induced by both brain IFN-alpha and IL-1beta is due to an activation of CRF system which leads to an enhancement of the SSN.(4) EP1 receptors for PGE2 are partly involved in the activation of brain CRF system. (5) The medial preoptic area (MPO) , which is the most potent acting site of IFN-alpha, is involved in the central regulation of immunity by its suppressive influence on the SSN.(6) Splenic NK activity decreases during dynamic phase of the ventromedial hypothalamus (VMH) lesiong-induced hyperphagia, while it increases during static phase. (7) An expression of c-fos protein in the MPO is important in thermoregulation during an exposure to high temperature. (8) An expression of IFN-alpha mRNA enhances by the immoblization stress in mouse. (9) Neurons in the anteroventral region of the III ventricle projecting to the MPO and the paraventricular nucleus play an important role in blood-borne cytokine-brain signal transduction. (10) Inhibition of the dorsal vagal motoneurons by IL-1beta through the prostanoids is considered to be one of the mechanisms of the IL-1beta-induced suppression of gastric acid secretion. (11) TNF-alpha inhibits the VMH neuronal activity, while TNF-beta activates it. (12) IFN-alpha suppresses the NMDA-induced inward current through the second mediators such as superoxide and nitric oxide. (13) The suppression of the NMDA-induced responses by IFN-alpha occurs only in the presence of the glial cells. PGE2 enhances the Ca^<2+> dependent K^+ current induced by glutamate. (14) IL-6 suppresses the long term potentiation in the hippocampal CA1 region.
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