Enhanced hippocampal neurodegeneration after traumatic or kainate excitotoxicity in GFAP-null mice. |
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Authors: | Naoki Otani Hiroshi Nawashiro Shinji Fukui Hidetoshi Ooigawa Atsushi Ohsumi Terushige Toyooka Katsuji Shima Hiroshi Gomi Michael Brenner |
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Institution: | Department of Neurosurgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan. gra006@ad.ndmc.ac.jp |
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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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