| Project/Area Number |
15K06715
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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 | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
吉原 誠一 奈良県立医科大学, 医学部, 講師 (90360669)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 嗅球 / ニューロン新生 |
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| Outline of Final Research Achievements |
The olfactory bulb (OB) possesses a battery of interneurons, including various types of granule cells (GCs); however, the contribution that each type of interneuron makes to the control of olfactory behavior remains unknown. Here, we investigated the function of the GC subtype (5T4 GCs), expressing oncofetal trophoblast glycoprotein 5T4. 5T4 facilitates the dendritic arborisation in the 5T4 GCs. Optogenetic stimulation of 5T4 GCs revealed their connection to external tufted cells (ETCs). Interestingly, in 5T4 knockout mice, ETCs received fewer inhibitory inputs from 5T4 GC dendrites than in the wild type. Notably, in olfactory behavior tests, 5T4 knockout mice had higher odor-detection thresholds than the wild type, as well as defects in odor-discrimination learning. Taken together, our findings suggest that loss of 5T4 attenuates inhibitory inputs from 5T4 GCs to ETCs, thus probably leading to superfluous firing of the ETCs and consequent disturbances in olfactory behaviors.
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