Mechanisms of basal ganglia control of thalamocortical activity
| Project/Area Number |
25430021
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
CHIKEN Satomi 生理学研究所, システム脳科学研究領域, 助教 (30396262)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 大脳基底核 / 視床 / 運動制御 / 神経活動 / サル / 神経活動記録 / マカクサル / 大脳皮質 |
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| Outline of Final Research Achievements |
The basal ganglia receive inputs from the cerebral cortices and project back to the original cortices via the thalamus, and control voluntary movements. Thus, for elucidating roles of these structures on voluntary movements, it is crucial to understand how their outputs control thalamocortical activity. We recorded activity of identified thalamocortical neurons projecting to the motor cortices of macaque monkeys, and examined responses to electrical stimulation of the internal segment of the globus pallidus (GPi), output nucleus of the basal ganglia.
During repetitive GPi stimulation at 50 or 100 Hz, each stimulus pulse evoked short-latency inhibition and following excitation. Local injection of gabazine, GABA-A receptor antagonist, in the vicinity of recorded neurons abolished both the inhibition and excitation without significant changes of spontaneous firing. The results suggest that basal ganglia outputs convey information through postinhibitory rebound excitation.
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Report
(4 results)
Research Products
(18 results)
