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Increase glial glutamate release couse to depression in rat model

Research Project

Project/Area Number 16K19774
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Psychiatric science
Research InstitutionUniversity of Miyazaki

Principal Investigator

ebihara kosuke  宮崎大学, 医学部, 助教 (20510720)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywordsグリア / 光遺伝学 / ICSS / 精神医学 / 行動科学
Outline of Final Research Achievements

I had negative results in this plan of experiment. I tried to discuss about some problem in this work. Maybe it is wrong potion in rat brain or method. Glutamine nerves are rich in prefrontal cortex. so aiming the point. but Glutamate receptor are beyond nerve endings, amygdala, including limbic system. Probably, Optogenetically stimulating amygdala increase glutamete and couse to beanhedonia in rat model.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • Research Products

    (1 results)

All 2017

All Presentation (1 results)

  • [Presentation] 光遺伝学的手法を用いたうつ病グリアモデルの検討2017

    • Author(s)
      蛯原 功介
    • Organizer
      日本生物学的精神医学会
    • Related Report
      2017 Annual Research Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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