| Project/Area Number |
16K20969
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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 |
Nerve anatomy/Neuropathology
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Yamada Kaoru 東京大学, 大学院医学系研究科(医学部), 助教 (00735152)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | α-synuclein / 伝播 / 神経活動 / 神経科学 |
|---|
| Outline of Final Research Achievements |
The pathological aggregation of α-synuclein characterizes a set of neurodegenerative disorders collectively referred to as α-synucleinopathies.α-Synuclein is a cytoplasmic protein, however, it is actively released into the extracellular space. In this study, utilizing in vivo microdialysis and primary neuronal culture, we demonstrated that physiological release of a-synuclein highly depends on neuronal activity. Selective modulation of glutamatergic neurotransmission altered extracellular α-synuclein levels in freely moving mice. While neuronal activity tightly regulated α-synuclein release, elevated synaptic vesicle exocytosis per se sfficiently elicited α-synuclein release. We also found that extracellular α-synuclein in brain interstitial fluid existed as 60kda high molecular weight species.
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