| Project/Area Number |
24590219
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Medical pharmacy
|
|---|
| Research Institution | Meijo University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MOURI Akihiro 名城大学, 薬学部, 助教 (20597851)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
NABESHIMA Toshitaka 名城大学, 薬学部地域医療薬局学講座 (70076751)
OZAKI Norio 名古屋大学, 大学院医学研究科精神医学 (40281480)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | 統合失調症 / モデルマウス / プロスタグランジンE2 / 環境要因 / 遺伝要因 / コピー数変異解析 / DISC 1 / モデル動物 / 認知機能 / 神経発達異常 / ドパミン / フェンシクリジン / グルタミン酸トランスポーター |
|---|
| Outline of Final Research Achievements |
We investigated the possibility of prostaglandin E2 (PGE2) as a common molecule associated with vulnerability to schizophrenia. PGE2 levels in whole brain were increased after injection of polyinosinic-polycytidylic acid (polyI:C), exposure to CO2, and separation, which are predisposing environmental factors, neonatally. The mice administered polyI:C or PGE2 neonatally exhibited the impairments of emotion/cognition, and the cortical dopaminergic in adult. PGE2 inhibited the neurite growth in the hippocampal neurons. These behavioral and neuronal impairments were not observed in the EP1 knockout mice. The mice administrated PGE2 neonatally were vulnerable to PCP-induced behaviors. In the copy number variants of PGE2-related genes, duplication at Ptges3 was only observed in one schizophrenic patient. In conclusion, PGE2 would be one of potential common molecule associated with environmental rather than genetic vulnerability to schizophrenia.
|
