| Project/Area Number |
26670536
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
KAWABATA Rika 金沢大学, 医学系, 研究員 (70726207)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | モデルマウス / 脳神経疾患 / 遺伝子改変マウス |
|---|
| Outline of Final Research Achievements |
In schizophrenia, alterations in the subset of cortical inhibitory neurons that express parvalbumin (PV) have been indicated by reduced expression of PV and GAD67, an enzyme for GABA synthesis, in these neurons. These alterations were accompanied by reduced expression of GABA-A receptor α1 (GABA-Aα1) subunit that mediates inhibitory neurotransmission by PV neurons. We tested a causal relationship between the changes in PV neurons and GABA-Aα1 expression through analyzing cortical gene expression in genetically engineered mice. In GABA-Aα1 knockout mice, we did not detect a significant change in GAD67 or PV mRNAs. Conversely, in mice with a conditional knockout of GAD67 in PV neurons, GABA-Aα1 mRNA expression was unaltered. These results did not support a relationship between the changes in PV neurons and GABA-Aα1 expression in the cortex of subjects with schizophrenia. There might be a common upstream mechanism that drives both changes in cortical inhibition in schizophrenia.
|
