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2018 Fiscal Year Final Research Report

Study of neuronal activity, a molecular basis and a behavioral change related to chemoreceptor-mediated nausea and emesis.

Research Project

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Project/Area Number 16K11471
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Functional basic dentistry
Research InstitutionHokkaido University

Principal Investigator

FUNAHASHI MAKOTO  北海道大学, 歯学研究院, 教授 (80221555)

Co-Investigator(Kenkyū-buntansha) 久留 和成  北海道大学, 歯学研究院, 助教 (00592081)
前澤 仁志  北海道大学, 歯学研究院, 助教 (80567727)
Project Period (FY) 2016-04-01 – 2019-03-31
Keywords悪心 / 嘔吐 / 最後野 / 迷走神経 / 化学受容器 / ラット
Outline of Final Research Achievements

As an intracellular mechanism for glucose responsiveness of the area postrema neurons, it was found that the ATP-dependent potassium channel (KATP channel) was closed by an increase in the extracellular glucose concentration, leading to the generation of depolarization and action-potentials. The glucose-responsive neurons were suggested to be H-channel non-expressing cells. The neuronal activity of the area postrema is crucial for the inducing mechanism of emetine-induced nausea, and it was also found that depolarization occurs in the central neurons including the nucleus tractus solitarius, the central nucleus of amygdala, the bed nucleus. It became clear that the memory recall of the taste aversion did not involve the activity of the nervous system related to a nausea induction.

Free Research Field

口腔生理学

Academic Significance and Societal Importance of the Research Achievements

本研究成果は化学受容性悪心・嘔吐の中枢機序について,延髄最後野のニューロン活動および連携する中枢ニューロン活動に着目して実験を行い,これまで不明であった点を明らかにして新たな概念を樹立するための基礎となる知見を得たものであり,その学術的意義は深い。また,抗がん剤の副作用による悪心・嘔吐の機序解明と新たな制吐方法の創出や制吐薬の開発につながる点では社会的意義が深い。

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Published: 2020-03-30  

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