2019 Fiscal Year Final Research Report
Molecular basis for the imprinted memory
Project/Area Number |
17K19386
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Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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Allocation Type | Multi-year Fund |
Research Field |
Biology of Cells to Organisms, and related fields
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Research Institution | University of Fukui |
Principal Investigator |
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Project Period (FY) |
2017-06-30 – 2020-03-31
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Keywords | 嗅覚 / 遺伝子改変マウス / 臨界期 / 刷り込み / 記憶 / シナプス形成 / 神経回路 / 神経科学 |
Outline of Final Research Achievements |
Sema7A/PlxnC1 signaling is key to inducing post-synaptic events within glomeruli in the mouse olfactory system. Odor exposure in neonates increases Sema7A expression in the responding glomeruli to promote primary-dendrite selection of mitral/tufted cells. This enhancement establishes imprinted odor memory that increases the sensitivity to the conditioned odorant and reduces stress reactions as adults. Imprinting does not occur when conditioning is performed after the critical period or in the absence of Sema7A/PlxnC1 signaling. We found that the imprinted odor activates the anterior medial-amygdala that mediates attractive social responses. Blockage of Sema7A/PlxnC1 signaling in neonates causes impairment of odor-mediated social behaviors, leading to abnormal avoidance of unfamiliar mice. Knockout and rescue experiments indicate that oxytocin in neonates is needed for imposing the positive quality on imprinted odor memory and for smooth social interactions as adults.
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Free Research Field |
神経科学
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Academic Significance and Societal Importance of the Research Achievements |
嗅覚系の刷り込み現象を明らかにした本研究の成果は、百年以上前から広く知られているが未解明であった刷り込み現象、例えばアヒルのヒナが孵化後に初めて見た動く物体を親と記憶して生涯追従する行動や、サケ・マスが産卵のために生まれた支流に戻って来る母川回帰行動などにも敷衍でき、刷り込み現象を分子・神経回路レベルで理解する突破口となった。将来的には、臨界期における適切な感覚刺激や体験の欠如が、ヒトの精神発達障害、特に愛着障害や自閉症を引き起こす原因の理解へと繋がり、予防法や新たな治療法の開発に役立つと期待される。
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