| Project/Area Number |
22800081
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Nerve anatomy/Neuropathology
|
|---|
| Research Institution | Doshisha University (2011)
National Institute for Physiological Sciences (2010) |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,146,000 (Direct Cost: ¥2,420,000、Indirect Cost: ¥726,000)
Fiscal Year 2011: ¥1,508,000 (Direct Cost: ¥1,160,000、Indirect Cost: ¥348,000)
Fiscal Year 2010: ¥1,638,000 (Direct Cost: ¥1,260,000、Indirect Cost: ¥378,000)
|
|---|
| Keywords | 自閉症 / シナプス接着因子 / neuroligin / neurexin |
|---|
| Research Abstract |
In this research project, I studied the synaptic functions electrophysiologically in mutant mice that possess a single amino acid mutation of a synaptic adhesion molecule neuroligin that was found in human autism patients as well as in wild type neurons in which neuroligin expression was suppressed by RNA interference. In the somatosensory cortex, both single amino acid mutation and knock-down of neuroligin led to an imbalance between excitatory and inhibitory synaptic inputs. Moreover, it was found that the late phase of long-term potentiation in the hippocampus was selectively impaired in the knock-in mice.
|
