2022 Fiscal Year Final Research Report
Study on the neuronal mechanisms for the induction of depression and anxiety focusing on plastic changes in neurotransmission in the bed nucleus of the stria terminalis
Project/Area Number |
20H03389
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Review Section |
Basic Section 47040:Pharmacology-related
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Research Institution | Hokkaido University |
Principal Investigator |
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 不安 / 抑うつ / 分界条床核 / 慢性痛 / ストレス / 情動 |
Outline of Final Research Achievements |
The results of this study demonstrate the following neural mechanisms by which chronic pain induces anxiety: 1) chronic pain increases the excitability of intrinsic inhibitory neurons in the bed nucleus of the stria terminalis (BNST), 2) activation of intrinsic BNST neurons increases inhibitory synaptic inputs to the BNST neurons projecting to the lateral hypothalamus (LH), and 3) the reduced outputs from the BNST to the LH impairs downstream neurotransmission that in turn induces anxiety. Furthermore, this study shows the possibility that the neurons projecting from the lateral parabrachial nucleus transmit pain information to BNST neurons. We also found that about half of the BNST neurons projecting to the LH also project to the ventral tegmental area (VTA), and about half of the BNST neurons projecting to the VTA also project to the LH.
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Free Research Field |
神経薬理学
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Academic Significance and Societal Importance of the Research Achievements |
本研究成果から、慢性痛時に分界条床核から外側視床下部や腹側被蓋野に投射する神経の活動が抑制されることにより、抑うつや不安などの負情動が惹起されることが示された。本研究成果は、慢性痛による不安・抑うつの惹起に関与する神経基盤の一端を明らかにしたものであり、国際的にも高く評価される学術誌に掲載された。また、これらの知見は、不安障害やうつ病などの精神疾患の神経機構解明や治療薬開発に資することが期待される。
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