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  • Title: Enhanced hippocampal neurodegeneration after traumatic or kainate excitotoxicity in GFAP-null mice.
    Author: Otani N, Nawashiro H, Fukui S, Ooigawa H, Ohsumi A, Toyooka T, Shima K, Gomi H, Brenner M.
    Journal: J Clin Neurosci; 2006 Nov; 13(9):934-8. PubMed ID: 17085299.
    Abstract:
    Astrocytes perform a variety of functions in the adult central nervous system. Recent evidence suggests that the upregulation of glial fibrillary acidic protein (GFAP), an astrocyte-specific intermediate filament component, is a biological marker of neurotoxicity after cerebral injury. We herein compared the response to traumatic brain injury or kainic acid (KA)-induced neurotoxicity in GFAP knockout (GFAP-KO) and wild-type (WT) mice. Seventy-two hours after injury, all GFAP-KO mice showed hippocampal CA3 neurodegeneration, whereas WT mice did not show neurodegeneration. Seventy-two hours after KA administration, GFAP-KO mice were more susceptible to KA-induced seizures and had an increased number of pyknotic damaged CA3 neurons than did WT mice. These results indicate that GFAP plays a crucial role in pyramidal neuronal survival after injury or KA-induced neurotoxicity.
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