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• W1932209067 endingPage "248" @default.
• W1932209067 startingPage "241" @default.
• W1932209067 abstract "Oxidative stress produces neurotoxicity often related with various CNS disorders. A phosphatase inhibitor enhances the actions of the signaling kinases. Protein kinases mediated-action shows the neural protection in brain injury. Phosphatase inhibitor, okadaic acid (OA), may enhance the protection effect and benefit to improve neuronal plasticity in post-injury. Thus, we investigated that the protein prophatase inhibitor affects neuroprotective signaling and neuroplastic changes in hippocampus after oxidative injury. Electrophysiological and biochemical assays were used to observe changes in synaptic efficacy following electrical and/or pharmacological manipulation of synaptic function. Neuronal cell death, as assessed by propidium iodide (PI) uptake, was reduced by OA treatment (24 and 48 h) compared with KA treatment. The pattern of DCFH-DA fluorescence in hippocampal slices corresponded well with PI uptake. The phospho-AKT/AKT ratio showed that the level of phospho-AKT was significantly increased in the OA-treated group. Furthermore, the OA-treated group exhibited significantly increased expression of SOD2 compared with the KA-only group. Optical imaging revealed that KA treatment tended to delay the latency of electrical stimulation and decrease the amplitude of optical signals of synaptic activity. These results suggest that OA may protect hippocampal neurons against oxidative stress and the survived neurons may functional to synaptic plasticity changes." @default.
• W1932209067 created "2016-06-24" @default.
• W1932209067 creator A5017201856 @default.
• W1932209067 creator A5048145361 @default.
• W1932209067 creator A5066889380 @default.
• W1932209067 date "2015-08-01" @default.
• W1932209067 modified "2023-10-18" @default.
• W1932209067 title "Neuroprotective effects of okadaic acid following oxidative injury in organotypic hippocampal slice culture" @default.
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• W1932209067 doi "https://doi.org/10.1016/j.brainres.2015.05.039" @default.
• W1932209067 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26067888" @default.
• W1932209067 hasPublicationYear "2015" @default.
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