| 研究実績の概要 |
A transient anoxia can be mimicked in slices as anoxia-induced long-term potentiation (aLTP) of glutamate release. Although nitric oxide (NO) is responsible for aLTP induction, the site of NO production is unclear as well as the mechanism by which aLTP is expressed and maintained for a long period.
We identified that NO is released from both pyramidal neurons and nearby astrocytes. We also found that elevated NO switches on a positive feedback loop for its regenerative production. Once aLTP is expressed, it occludes activity-dependent LTP, which however can be rescued by blocking the regenerative loop of NO production.
These results offer a therapeutic possibility of rescuing patients from memory deficit after exposure to anoxia.
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