Molecular mechanism of inflammation-induced depression
| Project/Area Number |
25670510
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Chiba University |
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Principal Investigator |
HASHIMOTO KENJI 千葉大学, 社会精神保健教育研究センター, 教授 (10189483)
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| Research Collaborator |
ZHANG Ji-chun 千葉大学, 社会精神保健教育研究センター, 特任助教 (00733320)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脳神経疾患 / 炎症 / うつ病 / ニコチン受容体 / 脳由来神経栄養因子 / スパイン / 精神疾患 |
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| Outline of Final Research Achievements |
Although alpha-7 nicotinic acetylcholine receptor (nAchR), a subtype of nicotine receptors, plays a role in the inflammation, the role of alpha-7 nAChR in depression has been unknown. In this study, we examined the role of alpha-7 nAChR in depression using alpha-7 nAChR KO mice. We found that alpha-7 nAChR KO mice show depression-like phenotype, including anhedonia. We also found an increase of brain-derived neurotrophic factor (BDNF) in the nucleus accumbens, but not other regions (prefrontal cortex and hippocampus). Furthermore, TrkB antagonist ANA-12, but not TrkB agonist 7,8-DHF, showed antidepressant-like effects in alpha-7 nAChR KO mice. These findings suggest that increased BDNF-TRkB signaling in the nucleus accumbens, but not other brain regions, plays a key role in depression-like behavior in alpha-7 nAChR KO mice.
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Report
(3 results)
Research Products
(6 results)
