Abstract : One of the most vulnerable areas to ischemia or hypoglycemia is CA1 hippocampal region due to pyramidal neurons death. Glutamate receptors are involved together with protein-kinase C and nitric oxide synthase. Long-term potentiation (LTP) is generated in anoxic or hypoglycemic conditions via activation of NMDA while inhibition of these receptors attenuates this response. Protein-kinase C and nitric oxide synthase are involved in anoxic LTP mechanism. Postischemic neurons are hyperexcitable in CA3 area while CA1 pyramidal neurons degenerate and disappear. Changes of glutamate receptors triggered by ischemia and hypoglycemia are discussed in this review.
Type de document :
Article dans une revue
Journal of Cellular and Molecular Medicine, Wiley Open Access, 2003, 7 (4), pp.401-7
https://www.hal.inserm.fr/inserm-00484795
Contributeur : Roman Tyzio
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Soumis le : mercredi 19 mai 2010 - 11:02:26
Dernière modification le : jeudi 7 février 2019 - 14:23:26
Document(s) archivé(s) le : jeudi 1 décembre 2016 - 00:16:43
Valérie Crepel, Jérôme Epsztein, Yehezkel Ben-Ari. Ischemia induces short- and long-term remodeling of synaptic activity in the hippocampus.. Journal of Cellular and Molecular Medicine, Wiley Open Access, 2003, 7 (4), pp.401-7. 〈inserm-00484795〉
