Strong expression of GFAP mRNA in rat hippocampus after a closed-head injury

Bodjarian, Nadia; Jamali, Samir; Boisset, Nazaire; Tadié, M

doi:10.1097/00001756-199712220-00020

Cited by 10 publications

(8 citation statements)

References 11 publications

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“…Reactive astrocytes had a distinct morphology characterized by an enlarged cell body and long intertwined processes. Our findings were consistent with Bodjarian et al 's study, in that they demonstrated increased GFAP mRNA expression after closed head injury where more intense and rapid expression was noted in the hippocampus 20…”

Section: Discussionsupporting

confidence: 93%

Marked Hippocampal Neuronal Damage without Motor Deficits after Mild Concussive‐like Brain Injury in Apolipoprotein E‐deficient Mice

Han

Chung²

2000

Annals of the New York Academy of Sciences

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Of various biological factors, only allele epsilon 4 of apolipoprotein E (apoE, protein; APOE4, gene) has been thus far suggested as a major determinant of genetic risk for sporadic and late-onset familial Alzheimer's disease (AD). Environmental influences such as lack of education, traumatic brain injury, oxidative stress, environmental toxins, hormonal imbalances, and alterations in immune or inflammatory responses may also contribute to the pathogenesis of AD. Thus genetic susceptibility and environmental risk factors may have synergistic effects on the development of AD. The purpose of present report was to assess whether the gene (APOE) and the environmental risk factor (traumatic brain injury) could interact in hippocampal neuronal degeneration. We investigated the histopathological changes of hipoccampal regions after mild concussive-like brain injury without motor deficits in apoE-deficient mice using the recently described novel weight-drop device. Control mice revealed minimal neurodegenerative changes limited to CA2 and CA3, while apoE-deficient mice showed widespread neuronal degeneration throughout hippocampal subfields and part of dentate gyrus. We also observed widespread glial fibrillary acidic protein (GFAP) immunoreactivity throughout the hippocampus, which was more intense in apoE-deficient mice. The results of this study indicate that even very mild traumatic brain injury could result in widespread hippocampal damage in apoE-deficient mice. This again supports the hypothesis that apoE might play a neurotrophic or neuroprotective function in the central nervous system.

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Section: Discussionsupporting

confidence: 93%

Marked Hippocampal Neuronal Damage without Motor Deficits after Mild Concussive‐like Brain Injury in Apolipoprotein E‐deficient Mice

Han

Chung²

2000

Annals of the New York Academy of Sciences

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“…Several markers or changes in human brain tissue after traumatic brain injury have been investigated using immunohistochemistry [28, 61,62,63,64,65,66,67,68,69]. In experimental brain injury models, the detection of several different markers has been reported from between 1 h to 1 day after injury [70,71,72,73,74,75]. DAI can be found in cases that sustained mild traumatic brain injury with no macroscopic changes at autopsy.…”

Section: Discussionmentioning

confidence: 99%

Real-time PCR quantitation of FE65 a β-amyloid precursor protein-binding protein after traumatic brain injury in rats

et al. 2003

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In cases of traumatic brain injury (TBI) in which the patient survived for only a short period of time and was without macroscopic changes at autopsy, it is difficult to diagnose TBI. To detect early diagnostic markers of diffuse axonal injury (DAI), real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) in an experimental head trauma model of rat was chosen. The β-amyloid precursor protein (β-APP) is a well-known diagnostic marker of DAI which can be detected by immunolabeling as early as 1.5 h after injury. β-APP has a binding protein, FE65, which is expressed in the brain of Alzheimer's disease patients along with β-APP, but no involvement with brain injury has been reported. Neuronspecific enolase (NSE) is also a useful marker of DAI. We found that FE65 expression increased dramatically as early as 30 min after injury and decreased after peaking 1 h postinjury, although NSE showed no significant changes. These results suggest that real-time PCR of FE65 mRNA is useful for the diagnosis of DAI in forensic cases.

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“…A possible source of error in estimating NAA reduction at later time points is possible change in nonneuronal protein due to posttraumatic glial hypertrophy and invasion. Nevertheless, in this model of trauma, with no secondary insult, these phenomena are of limited importance in accounting for a 50% NAA reduction at 48 h (Bodjarian et al, 1997;Dietrich et al, 1999;Ito et al, 1996).…”

Section: N-acetylaspartate Reduction After Traumatic Brain Injurymentioning

confidence: 98%

N-Acetylaspartate Reduction as a Measure of Injury Severity and Mitochondrial Dysfunction Following Diffuse Traumatic Brain Injury

Signoretti

Marmarou

Tavazzi

et al. 2001

Journal of Neurotrauma

200

134

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N-Acetylaspartate (NAA) is considered a neuron-specific metabolite and its reduction a marker of neuronal loss. The objective of this study was to evaluate the time course of NAA changes in varying grades of traumatic brain injury (TBI), in concert with the disturbance of energy metabolites (ATP). Since NAA is synthesized by the mitochondria, it was hypothesized that changes in NAA would follow ATP. The impact acceleration model was used to produce three grades of TBI. Sprague-Dawley rats were divided into the following four groups: sham control (n = 12); moderate TBI (n = 36); severe TBI (n = 36); and severe TBI coupled with hypoxia-hypotension (n = 16). Animals were sacrificed at different time points ranging from 1 min to 120 h postinjury, and the brain was processed for high-performance liquid chromatography (HPLC) analysis of NAA and ATP. After moderate TBI, NAA reduced gradually by 35% at 6 h and 46% at 15 h, accompanied by a 57% and 45% reduction in ATP. A spontaneous recovery of NAA to 86% of baseline at 120 h was paralleled by a restoration in ATP. In severe TBI, NAA fell suddenly and did not recover, showing critical reduction (60%) at 48 h. ATP was reduced by 70% and also did not recover. Maximum NAA and ATP decrease occurred with secondary insult (80% and 90%, respectively, at 48 h). These data show that, at 48 h post diffuse TBI, reduction of NAA is graded according to the severity of insult. NAA recovers if the degree of injury is moderate and not accompanied by secondary insult. The highly similar time course and correlation between NAA and ATP supports the notion that NAA reduction is related to energetic impairment.

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Strong expression of GFAP mRNA in rat hippocampus after a closed-head injury

Cited by 10 publications

References 11 publications

Marked Hippocampal Neuronal Damage without Motor Deficits after Mild Concussive‐like Brain Injury in Apolipoprotein E‐deficient Mice

Marked Hippocampal Neuronal Damage without Motor Deficits after Mild Concussive‐like Brain Injury in Apolipoprotein E‐deficient Mice

Real-time PCR quantitation of FE65 a β-amyloid precursor protein-binding protein after traumatic brain injury in rats

N-Acetylaspartate Reduction as a Measure of Injury Severity and Mitochondrial Dysfunction Following Diffuse Traumatic Brain Injury

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