Na+, K+-ATPase dysfunction in the pathophysiology of anxiety: Involvement of brain-kidney crosstalk
| Project/Area Number |
17K15458
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pharmacology in pharmacy
|
|---|
| Research Institution | Kumamoto University |
|---|
Principal Investigator |
Kurauchi Yuki 熊本大学, 大学院生命科学研究部(薬), 助教 (70631638)
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 脳-腎連関 / 不安 / 社会性 / Na+,K+-ATPase / 酸化ストレス / レドックス / Na+, K+-ATPase / 不安障害 / 脳血管障害 |
|---|
| Outline of Final Research Achievements |
Chronic kidney disease (CKD) patients shows psychiatric symptoms such as depression. In this study, 5/6-nephrectomized model mice (CKD model mice) were produced and were performed behavioral test focusing psychiatric symptoms. At eight weeks after the surgery, anxiety level of CKD model mice was higher than sham mice (Elevated plus maze test and light/dark box test). In addition, CKD model mice showed lower sociability than sham mice (sociability test). Furthermore, we observed glial activation and the increase in oxidative stress level in the brain of CKD model mice. These results suggest that renal dysfunction, followed by glial activation in the brain, contributes to the pathophysiology of psychiatric symptoms of CKD patients.
|
| Academic Significance and Societal Importance of the Research Achievements |
CKD患者はうつ病などの精神症状を合併することが多いが、その発症メカニズムは解明されていない。本研究では、CKDの代表的な病態モデルである5/6腎臓摘出モデルマウスの詳細な行動解析および生化学的解析により、CKDモデルマウスの不安レベルが高く、社会性が低下していることを明らかにした。本研究は、CKD患者が合併する精神症状の発症機序解明のみならず、高齢化に伴い増加し続けると予想されるCKD患者の身体および精神状態の包括的マネジメントにつながると考える。
|
Report
(3 results)
Research Products
(50 results)
