2021 Fiscal Year Final Research Report
Neural circuits involved in fear-induced physiological responess
Project/Area Number |
19K06773
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 44050:Animal physiological chemistry, physiology and behavioral biology-related
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Research Institution | Kansai Medical University |
Principal Investigator |
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | 恐怖情動 / 匂い物質 / trpa1 / 体温 / 代謝 |
Outline of Final Research Achievements |
Innate fear has evolved to orchestrate protective effects in crises by inducing behavioral and physiological responses. However, the mechanism by which physiological responses induced by innate fear stimuli contribute to the generation of bioprotective effects are mostly elusive. Thiazoline-related fear odors (tFOs), chemical analogs of predator odorants, induce robust innate fear and systemic hypothermia/hypometabolism in mice. Moreover, tFO-stimulation enables long-term survival in a lethal hypoxic environment and exerts therapeutic effects in cutaneous and cerebral ischemia/reperfusion injury models. Finally, we show that most of the tFO-induced responses are mediated by transient receptor potential ankyrin 1 (TRPA1), a receptor of tFOs, and brain stem Sp5/NST to midbrain PBN pathway.
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Free Research Field |
神経科学
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Academic Significance and Societal Importance of the Research Achievements |
恐怖情動はすべてのヒトに保存された情動であり、我々の生存に必須の役割を果たしていると考えられる。一方、これまで恐怖情動が持つ生存に有利に働く機能に着目しこれを利用する試みはほとんどなかった。本研究により、先天的な恐怖情動が誘発されたマウスでは低酸素耐性、虚血再灌流障害耐性など危機的状況下における生命保護作用が引き起こされることがわかってきた。このことは、ヒトにおいても恐怖情動誘発に関わる分子や神経回路に働きかけることで、低酸素障害や脳梗塞・心筋梗塞などの虚血再還流障害等の治療にも繋がる可能性が示唆された。
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