2018 Fiscal Year Final Research Report
The underlying mechanisms of synaptic dysfunction after the irradiation
| Project/Area Number |
17K16424
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Radiation science
|
|---|
| Research Institution | Gunma University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
Shirao Tomoaki
Takahashi Akihisa
Kawamura Hidemasa
Hanamura Kenji
Yamazaki Hiroyuki
Koganezawa Noriko
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Keywords | X-irradiation / cognitive impairment / synaptic dysfunction / drebrin / NMDA receptors |
|---|
| Outline of Final Research Achievements |
Previously we have shown that radiation may produce acute temporary cognitive impairment via decreases of postsynaptic protein drebrin from the synapse within 24 hours. In order to reveal the mechanisms radiation-induced synaptic dysfunction and its prevention, the ten-weeks-old C57BL/6N male mice were pretreated by injection of saline or N-methyl-D-aspartate (NMDA) receptor antagonist MK801 ten minutes before of a whole brain of irradiation, and then the immunoreactivity of postsynaptic protein drebrin was analysed on molecular layer of DG of Hippocampus 8 hours following X irradiation. Our results show there was a decrease in the immunoreactivity of drebrin and the N-methyl-D-aspartate (NMDA) receptor antagonist MK801 prevented it. These results indicate that the NMDA receptor mediates X-irradiation-induced drebrin decrease possibly via drebrin exodus.
|
| Free Research Field |
放射線神経生物
|
| Academic Significance and Societal Importance of the Research Achievements |
The effects of radiation on the CNS are of significant interest. In this study suggests that NMDAR-mediated drebrin reduction underlies X-irradiation-induced acute transient cognitive impairment, which may be a basis of further research for radiation protection on the brain.
|
