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- W2461024430 abstract "Long-term potentiation (LTP) has been widely studied as a form of synaptic plasticity that represents a cellular mechanism of learning and memory. Among numerous processes and molecules that may be involved in LTP formation, a great many of them including neurotrophic and transcription factors have been described as those involved in neural death after ischemic insult. Nitric oxide (NO) is a molecule that is known to also exert double-edged effects on LTP formation. Here we will be describing recent advances with respect to the LTP mechanisms in the hippocampal synapses, a critical brain region for learning and memory function. In another context, we described our study elucidating the changes in hippocampal LTP as a functional response to transient cerebral ischemic insult, from the viewpoint of its relevance to NO production. As indices of NO production, nitrite and nitrate levels were determined by in vivo microdialysis. It was demonstrated that hippocampal LTP deficiency after transient cerebral ischemia was preceded by an increase in hippocampal NO production. Direct or indirect inhibition of an inducible NO synthase restored ischemia-induced LTP deficiency. These findings suggest that NO production, in part via inducible NO synthase, is responsible for LTP deficiency after transient cerebral ischemia in the rat hippocampus." @default.
- W2461024430 created "2016-07-22" @default.
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- W2461024430 date "1998-01-01" @default.
- W2461024430 modified "2023-09-25" @default.
- W2461024430 title "Molecular Pathopharmacology of Cellular Responses to Brain Ischemia. Transient cerebral ischemia and long-term potentiation in the rat hippocampus." @default.
- W2461024430 doi "https://doi.org/10.1254/fpj.111.55" @default.
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- W2461024430 hasPublicationYear "1998" @default.
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