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2020 Fiscal Year Final Research Report

Elucidation of the Pathogenesis of Chronic Pain Focusing on Decreased Neuronal Generation in the Hippocampus.

Research Project

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Project/Area Number 18K08822
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 55050:Anesthesiology-related
Research InstitutionNagoya City University

Principal Investigator

SOBUE Kazuya  名古屋市立大学, 医薬学総合研究院(医学), 教授 (90264738)

Co-Investigator(Kenkyū-buntansha) 太田 晴子  名古屋市立大学, 医薬学総合研究院(医学), 講師 (90534751)
草間 宣好  名古屋市立大学, 医薬学総合研究院(医学), 講師 (60336691)
大澤 匡弘  名古屋市立大学, 医薬学総合研究院(薬学), 准教授 (80369173)
Project Period (FY) 2018-04-01 – 2021-03-31
Keywords慢性疼痛 / 海馬 / 神経細胞の新生低下
Outline of Final Research Achievements

The purpose of this study was to clarify the mechanism (neural circuits involved) and physiological significance of the decrease in hippocampal neurogenesis in chronic pain, and to examine the possibility that this is one of the causes of prolonged pain. We found that neuropathic pain-induced decrease in hippocampal neurogenesis involves a decrease in the number of neural progenitor cells in the subgranular zone (SGZ) of the hippocampal dentate gyrus and activation of the neural circuitry projecting from the spinal dorsal horn (SDH) to the lateral parabrachial nucleus (LPB). Since SDH-LPB nerves are negative affective circuits, the decrease in hippocampal neurogenesis due to stimulation involves activation of neural circuits that transmit the negative emotions of pain. In addition, we found that somatosensory neural circuits of pain are not involved in the decrease of hippocampal neurogenesis.

Free Research Field

麻酔科学、神経科学

Academic Significance and Societal Importance of the Research Achievements

本研究により、神経障害性疼痛による海馬の神経新生低下に、海馬歯状回の顆粒細胞下帯(SGZ)の神経前駆細胞数の低下や脊髄後角(SDH)から外側腕傍核(LPB)に投射する神経回路の活性化が関わることが明らかになった。これが痛みの遷延化の原因のひとつである可能性があり、今後の研究で慢性疼痛の治療法開発につながる可能性がある。

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Published: 2022-01-27  

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