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Stereotactic frame

Fig. 3. In vivo contusion injury devices. Injury devices are used to experimentally deliver prescribed injury parameters to the exposed brain or spinal cord. For example, the Infinite Horizons spinal cord contusion device (A) allows the user to select an impact force for injury, while the controlled cortical impact device (B) utilizes a pneumatic system to injure the brain at a defined tissue displacement.

Fig. 4. Acute cellular permeability following TBI and SCI. In the acute phase of traumatic injury, the plasma membrane becomes damaged due to local cellular strains that exceed structural thresholds. Lucifer yellow uptake in the injured brain (A) and spinal cord (B) demonstrates a heterogeneous distribution of membrane failure, suggesting that loading is not evenly distributed throughout the CNS parenchyma.

Fig. 4. Acute cellular permeability following TBI and SCI. In the acute phase of traumatic injury, the plasma membrane becomes damaged due to local cellular strains that exceed structural thresholds. Lucifer yellow uptake in the injured brain (A) and spinal cord (B) demonstrates a heterogeneous distribution of membrane failure, suggesting that loading is not evenly distributed throughout the CNS parenchyma.

lead to abnormal ion movement across the membrane, resulting in pathophysiological changes such as conduction block, neurofilament compaction, and impaired axonal transport (Pettus et al., 1994; Shi and Pryor, 2002). Thus, mechanical loading may directly result in pathophysiological changes.

Experimental evidence has demonstrated that the extent of membrane compromise is dependent on the magnitude and rate of strain (LaPlaca et al., 1997; Geddes et al., 2003; Shi and Whitebone, 2006). In addition, others have suggested that the mode of injury may play a critical role in dictating the extent of mechanically induced cell membrane damage (Geddes-Klein et al., 2006). After TBI, membrane disruption has been shown to occur after focal injury in a contusion model (Fig. 4) as well as diffuse loading after impact acceleration injury (Farkas et al., 2006), with patterns of marker uptake specific to the mode of impact. Because there is a correlation between injury severity and membrane compromise, permeability markers can therefore be used as an indicator of the extent of local cellular loading parameters. For example, experiments conducted in our laboratory have demonstrated more extensive permeability marker uptake in specific hippocampal regions after contusion injury, suggesting that local cellular loading is more severe in certain anatomical locations. These data may explain the preferential cell death seen in these regions in the subacute and chronic phases, as mechanical damage during the initial

confocal microscope 3-D Cell Shearing Device

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