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Traumatic brain injury-induced excitotoxicity assessed in a controlled cortical impact model

daniel123 添加于 2011-10-19 11:25 | 1883 次阅读 | 0 个评论

作者
Palmer AM, Marion DW, Botscheller ML, Swedlow PE, Styren SD, DeKosky ST
摘要
Using a controlled cortical impact model of traumatic brain injury (TBI) coupled with tissue microdialysis, interstitial concentrations of aspartate and glutamate (together with serine and glutamine) were assessed in rat frontal cortex. Histological analysis indicated that the severity of injury following severe TBI (depth of deformation = 3.5 mm) was approximately twice that occurring following moderate TBI (depth of deformation = 1.5 mm). Both groups demonstrated significant postinjury maximal increases in excitatory amino acid (EAA) concentration, which were proportional to the severity of injury. The mean +/- SEM fold increase in dialysate concentrations of aspartate was 38 +/- 13 (n = 5) for moderate TBI and 74 +/- 12 (n = 5) for severe TBI. Fold increases in glutamate concentrations were 81 +/- 26 and 144 +/- 23 for moderate and severe TBI, respectively. Although these increases normalized within 20-30 min following moderate TBI, concentrations of aspartate and glutamate took > 60 min to normalize after severe TBI. Changes in levels of nontransmitter amino acids were much smaller. Fold increases for serine concentrations were 4.6 +/- 0.6 and 7.6 +/- 1.7 in moderate and severe TBI, respectively; glutamine concentrations had similar small fold increases (2.6 +/- 0.2 and 4.1 +/- 0.6, respectively). Calculation of interstitial concentrations following severe TBI indicated that aspartate and glutamate maximally increased to 123 +/- 20 and 414 +/- 66 microM, respectively. To determine the extent to which such tissue concentrations of EAAs could contribute to the injury seen in TBI, the EAA receptor agonists N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid were slowly injected into rat cortex. Remarkably similar histological injuries were produced by this procedure, supporting the notion that TBI is an excitotoxic injury.
详细资料
- 文献种类:期刊
- 期刊名称: Journal of Neurochemistry
- 期刊缩写: J Neurochem
- 期卷页: 1993年第61卷第6期 2015-2024页
- 地址: Department of Psychiatry, University of Pittsburgh School of Medicine, Pennsylvania 15213
- ISBN: 0022-3042
- 备注:PMID:7504079
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