Investigation of pathogenic mechanisms for central post-stroke pain and its accompanying emotional disorder - evaluation of microglial activation hypothesis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10311
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurosurgery
• Research Institution: Kagoshima University
• Principal Investigator: ARITA Kazunori 鹿児島大学, 医歯学域医学系, 教授 (90212646)
• Co-Investigator(Kenkyū-buntansha): 時村 洋 鹿児島大学, 医歯学総合研究科, 客員研究員 (50227568) ; 宮田 篤郎 鹿児島大学, 医歯学域医学系, 教授 (60183969) ; 栗原 崇 鹿児島大学, 医歯学域医学系, 准教授 (60282745)
• Research Collaborator: SADAMURA Yuko ; SAMESHIMA Yoshimune
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 脳卒中後疼痛 / 視床痛 / ミクログリア / p38 MAPキナーゼ / 中枢神経障害性疼痛 / うつ様行動 / 不安様行動 / 電位依存性Caチャネル

Outline of Final Research Achievements

In this study, we have established experimental conditions that enabled us to measure both stable mechanical withdrawal thresholds of hindpaws and emotional behaviors of thalamic hemorrhage-induced central post-stroke pain model mice. We found that systemic administration of inhibitors for microglial activation including minocycline and p38 MAP kinase inhibitors significantly alleviated the expression of both thalamic hemorrhage-induced mechanical allodynia and increased locomotor activity. Furthermore, N-type voltage-gated Ca channels were suggested to contribute to the development of the thalamic hemorrhage-induced mechanical allodynia in the acute phase. In contrast, we have not yet detected significant thalamic hemorrhage-induced depression-like behaviors in both acute and subacute phases. Thus, further study is necessary for the detection of the depression-like behaviors.

Free Research Field

脳神経外科学分野