Time course of cellular pathology after controlled cortical impact injury

Chen, S; Pickard, John D.; Harris, Neil G.

doi:10.1016/s0014-4886(03)00002-5

Cited by 214 publications

(179 citation statements)

References 72 publications

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“…Although an increased number of glial cells have been observed in the ipsilateral white matter tracts following FP brain injury (Graham et al, 2000), our data are the first to suggest that the number of oligodendrocytes may increase in selected regions following TBI, as previously demonstrated in models of cerebral ischemia (Dewar et al, 2003;Zaidi et al, 2004), spinal cord injury (McTigue et al, 2001) and cortical resection brain injury (Ludwin, 1984). In a recent report, proliferation of oligodendrocyte precursors, that may differentiate into mature oligodendrocytes following CNS injury (McTigue et al, 2001), was observed in the acute period following experimental TBI (Chen et al, 2003). Since oligodendrocytes and oligodendro-cyte precursor cells have been suggested to exert an inhibitory effect on axonal outgrowth (Chen et al, 2002a,b), an increase in the number of oligodendrocytes may contribute to the lack of axonal regeneration in TBI.…”

Section: Discussionsupporting

confidence: 83%

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP-and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI. KeywordsNogo-A; Nogo-66 receptor; Small proline-rich repeat protein 1A (SPRR1A); Traumatic brain injury; Oligodendrocytes

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Section: Discussionsupporting

confidence: 83%

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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“…In a moderate controlled cortical impact injury model, mean density and diameter of cortical microvessels were significantly reduced and increased, respectively, in the contusion margin at the initial time points. 24 In our study, there was significant difference in vessels dilation on CDFI and hyperperfusion on CEUS in adjacent region. These vivid and realtime features by CDFI and CEUS provided strong evidence that vessel dilation in pericontusional region was a response to the mechanical insult and metabolic demand.…”

Section: Discussionsupporting

confidence: 43%

Quantitative assessment of spinal cord perfusion by using contrast-enhanced ultrasound in a porcine model with acute spinal cord contusion

et al. 2012

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Objectives: To quantify spinal cord perfusion by using contrast-enhanced ultrasound (CEUS) in a porcine model with acute spinal cord injury. Methods: Microcirculatory changes of acute spinal cord injury were shown by CEUS in a porcine model with spinal cord contusion at three selected time points, coupling with conventional ultrasound (US) and Color Doppler US (CDFI). Time-intensity curves and perfusion parameters were also obtained by autotracking contrast quantification (ACQ) software in the epicenter of contusion site, adjacent region and distant region, respectively. Neurologic and histologic examinations were used to confirm the severity of injury. Results: Conventional US revealed the spinal cord was hypoechoic and homogeneous, whereas the dura mater, pia mater and cerebral aqueduct were hyperechoic. On CDFI intramedullary blood vessels were displayed as segmental and columnar. It was homogeneous on CEUS. After spinal cord contusion, the injured region on gray scale US was hyperechoic. CDFI demonstrated intramedullary blood vessels of adjacent region had increased and dilated during the observation period. On CEUS the epicenter of contusion site was hypoperfusion, whereas its adjacent region was hyperperfusion compared with the distant region. Quantitative analysis showed that peak intensity decreased in epicenters of contusion but increased in adjacent regions significantly at all time points (Po0.05). Evaluation of neurological function for post-contusion demonstrated significantly deterioration in comparison before injury (Po0.05). Conclusions: CEUS is a practical technique that provides overall views for evaluating microcirculatory pattern in spinal cord injury. Quantitative analysis shows the efficacy in assessment of perfusion changes after spinal cord injury.

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“…This would be especially notable in the pial strip model in which tissue can move into not only the infarct, but also into the cavity produced by the trephination itself (Adams et al, 1994;Kolb & Holmes, 1983;Navari et al, 1978;Whishaw, 2000;Xu et al, 2007). Second, all of the stroke models likely involve neuroinflammatory responses, secondary neurodegeneration, and apoptosis, which take place over time following the stroke (Chen et al, 2003;Bidmon et al, 1998;Pulsinelli, 1982;Witte et al, 2000). Third, there are likely widespread changes involving the loss of neuropile and adjustments in surviving neurons that contribute to time-dependent cortical alterations (Butefisch, 2006;Jones, 1999;Jones et al, 1996Jones et al, , 1999.…”

Section: Discussionmentioning

confidence: 99%

“…These results again indicate that cortical areas beyond the stroke infarct are susceptible to anatomical changes at chronic post-stroke time periods. These changes include extension of intact tissue into the stroke core, which could contribute to thinning of distal residual tissue by stretching it, and/or by aggravating secondary neuronal degeneration processes known to occur after focal cortical brain injury (Chen et al, 2003).…”

Section: Residual Tissue Movement In Histological and Mri Sectionsmentioning

confidence: 99%

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

et al. 2010

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Time course of cellular pathology after controlled cortical impact injury

Cited by 214 publications

References 72 publications

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Quantitative assessment of spinal cord perfusion by using contrast-enhanced ultrasound in a porcine model with acute spinal cord contusion

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

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