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.
MeSH terms
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Animals
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Astrocytes / cytology
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Astrocytes / metabolism*
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Brain Injuries / complications*
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Brain Injuries / metabolism
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Brain Injuries / physiopathology
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Cell Communication / genetics
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Cell Survival / physiology
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Cytoprotection / genetics*
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Disease Models, Animal
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Drug Resistance / genetics
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Glial Fibrillary Acidic Protein / genetics*
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Hippocampus / drug effects
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Hippocampus / pathology*
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Hippocampus / physiopathology
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Kainic Acid / toxicity
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Nerve Degeneration / chemically induced
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Nerve Degeneration / genetics*
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Nerve Degeneration / metabolism
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Neurotoxins / toxicity
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Pyramidal Cells / drug effects
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Pyramidal Cells / pathology
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Recovery of Function / physiology
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Seizures / chemically induced
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Seizures / genetics
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Seizures / physiopathology
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Up-Regulation / drug effects
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Up-Regulation / genetics
Substances
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Glial Fibrillary Acidic Protein
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Neurotoxins
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Kainic Acid