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• W2025959962 abstract "Neurons from cerebral neocortex and hippocampus exhibit a striking difference in vulnerability to transient global ischemia. In order to study the contribution of neuronal connections and neuron–glia interactions to this variation in neuronal vulnerability, we used hippocampal and neocortical cultures submitted to various periods of histotoxic ischemia. Organotypic cultures were exposed at 37°C for 0, 7, 30 and 60 min to a glucose-free NaCN-containing medium. Histological analysis using thionin staining and MAP2 immunostaining showed differences in the temporal profile of neuronal damage in hippocampal and neocortical structures, i.e., in decreasing order, CA1 (7 min) > CA3 and neocortical layers II, III, V, VI (30 min) > DG and neocortical layer IV (60 min). In parallel to the neurodegeneration study, the time course and the regional pattern of microglial and astroglial changes were also examined using GS-B4 isolectin and GFAP as immunohistochemical markers, respectively. The GS-B4 isolectin staining revealed an early (at 7 min for the hippocampus) and a specific microglial activation located in areas undergoing neuronal damage. For both organotypic cultures, astrogliosis occurred later (after 30 min of stress) with no specific regional distribution. Both hippocampal and neocortical cultures submitted to histotoxic ischemia allowed the replication of many of the cellular events observed in response to global ischemiain vivo.These findings support the hypothesis that neuron–neuron connections as well as interactions between neurons and glial cells are essential to reproducein vitrothe selective neuronal vulnerability describedin vivo." @default.
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• W2025959962 date "1998-03-01" @default.
• W2025959962 modified "2023-09-25" @default.
• W2025959962 title "Selective Neuronal Vulnerability and Specific Glial Reactions in Hippocampal and Neocortical Organotypic Cultures Submitted to Ischemia" @default.
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• W2025959962 doi "https://doi.org/10.1006/exnr.1997.6728" @default.
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