Role of parabrachial-central amygdala system in inflammation-pain association

2023 Fiscal Year Final Research Report

• Project/Area Number: 21H02816
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 51030:Pathophysiologic neuroscience-related
• Research Institution: Jikei University School of Medicine
• Principal Investigator: Kato Fusao 東京慈恵会医科大学, 医学部, 教授 (20169519)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 慢性痛 / 炎症 / 中枢性感作 / 腕傍核 / 扁桃体中心核 / FosTRAP / 痛覚変調性疼痛 / オピオイド受容体

Outline of Final Research Achievements

We found that 1) brief local inflammation activates and causes plastic changes in the parabrachial-central amygdala system, 2) these plastic changes lead to nociplastic pain and result in long-lasting widespread hyperalgesia, 3) opioids markedly inhibit excitatory synaptic transmission between neurons in the parabrachial-central nucleus of the amygdala through presynaptic mechanisms. This might be a primary target of opioids for its analgesic effects and may also be a mechanism for preventing delayed chronic pain. 4) In the early phase of systemic inflammation, PBN-CeA synaptic transmission inhibition by endogenous opioids occurs, potentially suppressing hyperalgesia. The inflammatory activation accompanying nociception would determine the subsequent establishment of widespread chronic sensitization through activating the LPB-CeC system.

Free Research Field

Neurophysiology

Academic Significance and Societal Importance of the Research Achievements

侵害受容器の活性化とともに生じる炎症系の活性化は，腕傍核－扁桃体系の活性化を通じて，その後の慢性的な痛覚過敏の成立の鍵を握ることを明らかにした．今後の慢性痛予防と治療医大きな影響と示唆をもたらす研究成果である．