| Project/Area Number |
26860159
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | Nagoya University (2015-2017)
Kyoto University (2014) |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 発熱 / 摂食 / 代謝 / プロスタグランジン / 視床下部 / 体温調節 / 感染 |
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| Outline of Final Research Achievements |
Infection elicits a variety of central symptoms, such as fever, decreased appetite, and fatigue. However, the neural mechanisms underlying the infection-induced symptoms are unknown. In this study, I focused on preoptic area neurons that express prostaglandin EP3 receptors, which receive the pyrogenic mediator produced in response to infections. By using a technique to express reporter genes specifically in EP3 receptor-expressing neurons in the preoptic area, I revealed all the brain sites to which EP3 receptor-expressing preoptic neurons project their axons, and also electrophysiologically recorded activities of these neurons. Based on the data obtained from these analyses, I hypothesized that the medullary reticular neurons are involved in the infection-induced suppression of appetite. Further studies to test this hypothesis could lead to elucidation of the central neural circuit mechanisms of infection-induced symptoms.
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