Central circuit mechanisms underlying infection-induced food intake inhibition

2021 Fiscal Year Final Research Report

• Project/Area Number: 17K08568
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Environmental physiology(including physical medicine and nutritional physiology)
• Research Institution: Nagoya University
• Principal Investigator: Nakamura Yoshiko 名古屋大学, 医学系研究科, 講師 (60548543)
• Project Period (FY): 2017-04-01 – 2022-03-31
• Keywords: プロスタグランジン / 体温調節 / 恒常性

Outline of Final Research Achievements

Infection elicits a variety of central symptoms, such as fever, decreased appetite. However, the neural mechanism underlying the infection-induced food intake inhibition is unknown. In this study, I focused on preoptic area neurons that express prostaglandin EP3 receptors, which receive the pyrogenic mediator, prostaglandin E2, 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 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. I am currently testing this hypothesis to further elucidate the central neural circuit mechanisms of infection-induced symptoms.

Free Research Field

環境生理学

Academic Significance and Societal Importance of the Research Achievements

プロスタグランジンE2の受容体であるEP3を発現する視床下部の視索前野ニューロンは発熱のスイッチとなることが知られている。しかしながら視索前野のEP3発現ニューロンの神経生理学的特性や、発熱以外の生理反応に関わることは知られていない。本研究によって、視索前野のEP3発現ニューロンが発熱のみならず、その他の感染症状や生理反応にも関わることで生命の維持に重要な役割を果たしていることが示唆された。