Journal of neurotrauma
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Journal of neurotrauma · May 2009
Cerebral autoregulatory response depends on the direction of change in perfusion pressure.
The purpose of cerebral autoregulation is to keep cerebral blood flow constant during variations of cerebral perfusion pressure (CPP). Recently, the autoregulatory response was reported to be greater during arterial blood pressure (ABP) increase than during decrease following repeated induced changes in ABP in 14 brain-injured subjects. The goal of this study was to further investigate the asymmetry of autoregulation during spontaneous increases and decreases of CPP in a larger group of brain injury patients. ⋯ Despite this difference, upMx and downMx were strongly correlated with each other (R=0.82; p < 0.001). In conclusion, the autoregulatory response was significantly greater during increase than during decrease in CPP. The results may indicate non-linear behavior of cerebral autoregulation.
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Journal of neurotrauma · May 2009
Forced exercise as a rehabilitation strategy after unilateral cervical spinal cord contusion injury.
Evaluation of locomotor training after spinal cord injury (SCI) has primarily focused on hind limb recovery, with evidence of functional and molecular changes in response to exercise. Since trauma at a cervical (C) level is common in human SCI, we used a unilateral C4 contusion injury model in rats to determine whether forced exercise (Ex) would affect spinal cord biochemistry, anatomy, and recovery of fore and hind limb function. SCI was created with the Infinite Horizon spinal cord impactor device at C4 with a force of 200 Kdyne and a mean displacement of 1600-1800 microm in adult female Sprague-Dawley rats that had been acclimated to a motorized exercise wheel apparatus. ⋯ The BBB test showed no change with Ex at the end of the 8-week period, however hind limb grid performance was improved during weeks 2-4. Lesion size was not affected by Ex, but the presence of phagocytic and reactive glial cells was reduced with Ex as an intervention. These results suggest that Ex alone can influence the evolution of the injury and transiently improve fore and hind limb function during weeks 2-4 following a cervical SCI.
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Journal of neurotrauma · May 2009
A novel protein complex in membrane rafts linking the NR2B glutamate receptor and autophagy is disrupted following traumatic brain injury.
Hyperactivation of N-methyl-D-aspartate receptors (NRs) is associated with neuronal cell death induced by traumatic brain injury (TBI) and many neurodegenerative conditions. NR signaling efficiency is dependent on receptor localization in membrane raft microdomains. Recently, excitotoxicity has been linked to autophagy, but mechanisms governing signal transduction remain unclear. ⋯ Moderate TBI induced rapid recruitment and association of NR2B and pCaMKII to membrane rafts, and translocation of Beclin-1 out of membrane microdomains. Furthermore, TBI caused significant increases in expression of key autophagic proteins and morphological hallmarks of autophagy that were significantly attenuated by treatment with the NR2B antagonist Ro 25-6981. Thus, stimulation of autophagy by NR2B signaling may be regulated by redistribution of Beclin-1 in membrane rafts after TBI.