Journal of neurotrauma
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Journal of neurotrauma · Apr 2009
The long-term microvascular and behavioral consequences of experimental traumatic brain injury after hypothermic intervention.
Traumatic brain injury (TBI) has been demonstrated to induce cerebral vascular dysfunction that is reflected in altered responses to various vasodilators. While previous reports have focused primarily on the short-term vascular alterations, few have examined these vascular changes for more than 7 days, or have attempted to correlate these alterations with any persisting behavioral changes or potential therapeutic modulation. Accordingly, we evaluated the long-term microvascular and behavioral consequences of experimental TBI and their therapeutic modulation via hypothermia. ⋯ In contrast, data from the MWM task indicated that injured animals revealed persistent deficits in the spatial memory test performance, with hypothermia exerting no protective effects. Collectively, these data illustrate that TBI can evoke long-standing brain vascular and spatial memory dysfunction that manifest different responses to hypothermic intervention. These findings further illustrate the complexity of TBI and highlight the fact that the chosen hypothermic intervention may not necessarily exert a global protective response.
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Journal of neurotrauma · Apr 2009
Locomotor recovery after spinal cord lesions in the lamprey is associated with functional and ultrastructural changes below lesion sites.
While axonal regeneration continues to be the major focus of research into spinal injury, there is growing evidence for changes in functional properties below lesion sites. In this study we have used the lamprey, a model system for studying axonal regeneration after spinal injury, to examine whether functional and ultrastructural changes below lesion sites might also contribute to the recovery of locomotor function in this system. In the current study, the majority of the animals showed good functional recovery 10 weeks after lesioning, even when there was no physiological evidence for regeneration across the lesion site (although animals that recovered poorly always lacked regeneration). ⋯ There were also changes in synaptic ultrastructure, including a reduction of the synaptic gap and an increase in synaptic vesicle pools at asymmetric (putative excitatory) synapses. These results provide the first evidence for functional changes below lesion sites in the lamprey, and suggest that locomotor recovery reflects an interaction between regenerated axons and altered networks below lesion sites. The lamprey offers a tractable model system in which to investigate how interactions between altered locomotor networks and regenerated axons are organized to promote locomotor recovery.
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Journal of neurotrauma · Apr 2009
The temporal expression, cellular localization, and inhibition of the chemokines MIP-2 and MCP-1 after traumatic brain injury in the rat.
The expression of the neutrophil chemokine macrophage inflammatory protein-2 (MIP-2/CXCL2) and the monocyte chemokine monocyte chemotactic protein-1 (MCP-1/CCL2) have been described in glial cells in vitro but their origin following TBI has not been established. Furthermore, little is known of the modulation of these chemokines. Chemokine expression was investigated in male Sprague-Dawley rats following moderate lateral fluid percussion injury (LFPI). ⋯ MIP-2/CXCL2 and MCP-1/CCL2 are increased after injury, and neurons appear to be the source of this expression. Chemokine expression was selectively inhibited by dexamethasone. The implications of this are discussed.
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Spinal cord injury (SCI) launches a complex cascade of events that leads to progressive damage and loss of function. Compromise of plasma membrane integrity due to the mechanical impact is an acute event that may contribute to cellular dysfunction. Therefore, the objective of this study was to better understand the extent of acute plasma membrane damage associated with SCI as a function of injury severity and membrane defect size. ⋯ In addition, after moderate injury, cell bodies and axons (located up to 2 mm and 3 mm from the epicenter, respectively) took up significantly more of the 3-kDa and 10-kDa dextran permeability marker compared to sham controls. Permeable neuronal cell bodies exhibited a morphological appearance characterized by pericellular blebbing, suggesting that plasma membrane compromise is associated with pathophysiological cellular alterations. Collectively, these results enhance our understanding of acute SCI and provide targets for developing novel treatment strategies.