| 研究実績の概要 |
Previously we have shown that radiation may produce acute temporary cognitive impairment via decreases of postsynaptic protein drebrin from the synapse within 24 hours. To reveals the mechanisms radiation-induced synaptic dysfunction and its prevention, the mice were pretreated by injection of saline or N-methyl-D-aspartate (NMDA) receptor antagonist MK801 ten minutes before of a whole brain of ten-weeks-old C57BL/6N male mice, then we examine the synaptic function using drebrin, and PSD-95 immunoreactivity on DG of Hippocampus 8 hours following X irradiation. Our results show there was a decrease in the immunoreactivity of drebrin and prevented by MK801. Thus results indicate that indicates that NMDA receptor mediates X-irradiation-induced drebrin decrease possibly via drebrin exodus.
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