Journal of neurotrauma
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Journal of neurotrauma · Sep 2010
Comparative StudyNeuroprotective effects of hyperbaric oxygen treatment on traumatic brain injury in the rat.
This study was designed to evaluate the potential benefits of hyperbaric oxygen (HBO) in the treatment of traumatic brain injury (TBI). The right cerebral cortex of rats was injured by the impact of a 20-g object dropped from a predetermined height. The rats received HBO treatment at 3 ATA for 60 min after TBI. ⋯ Although multiple treatments started at 48 h significantly improved neurological behaviors and reduced brain injury, the overall beneficial effects were substantially weaker than those seen after a single treatment at 6 h. These results suggest that: (1) HBO treatment could alleviate brain damage after TBI; (2) a single treatment with HBO has a time limitation of 12 h post-TBI; and (3) multiple HBO treatments have the possibility to extend the post-TBI delivery time window. Therefore, our results clearly suggest the validity of HBO therapy for the treatment of TBI.
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Journal of neurotrauma · Sep 2010
Comparative StudyIntracranial pressure following penetrating ballistic-like brain injury in rats.
Penetrating ballistic brain injury involves a leading shockwave producing a temporary cavity causing substantial secondary injury. In response to the prevalence of this type of brain trauma in the military, a rat model of penetrating ballistic-like brain injury (PBBI) was established. This study focuses on cerebral physiological responses resulting from a PBBI, specifically the immediate and delayed changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). ⋯ By comparison, probe insertion alone did not produce the immediate ICP crisis (28.6 ± 9.1 mm Hg), and only a mild and sustained increase in ICP (13.5 ± 2.1 mm Hg) was observed in the following 3 h post-injury. Injury severity, as measured by lesion volume, brain swelling, and neurological deficits at 1, 3, and 7 days post-injury, also reflected the distinctive differences between the dynamics of the PBBI versus controls. These results not only reinforced the severe nature of this model in mimicking the ballistic effect of PBBI, but also established cerebral pathophysiological targets for neuroprotective therapies.
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Journal of neurotrauma · Sep 2010
Comparative StudyCompression alters kinase and phosphatase activity and tau and MAP2 phosphorylation transiently while inducing the fast adaptive dendritic remodeling of underlying cortical neurons.
In traumatic brain injury (TBI) there is often compression of the cerebral cortex. Using a rat epidural bead implantation model we found that mechanical compression distorted the dendrites of underlying cortical pyramidal neurons, and that the deformed dendrites regained straight morphology in 3 days. This was accompanied by a transient increase in the phosphorylation of microtubule-associated proteins (MAPs) at sites known to destabilize microtubules, including MAP2 from 30 min to 1 h, and tau from 10 min to 12 h following compression. ⋯ The temporal coincidence of these events suggests that alterations of phosphatase and kinase activity underlie MAP2 and tau phosphorylation, thus causing the compressed cortical neurons to remodel their dendrites, including the proximal segments. The rapid onset of these molecular changes demonstrates that compression causes cortical neurons to undergo active changes much early than expected. The large-scale structural changes that result can alter cortical function for an extended period of time.
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Journal of neurotrauma · Sep 2010
Comparative StudyCare of rats with complete high-thoracic spinal cord injury.
The complications of spinal cord injury (SCI) increase in number and severity with the level of injury. A recent survey of SCI researchers reveals that animal models of high SCI are essential. Despite this consensus, most laboratories continue to work with mid- or low-thoracic SCI. ⋯ Here we provide details of our animal care procedures, including acclimatization, housing, diet, antibiotic prophylaxis, surgical procedures, post-operative monitoring, and prevention of complications. In our laboratory, this comprehensive approach consistently produces good outcomes following T3 complete transection SCI: using body weight as an objective indicator of animal health, we have found that our rats typically return to pre-operative weights within 10 days of T3 complete SCI. It is our hope that the information provided here will improve care of experimental animals, and facilitate adoption of models that directly address the complications associated with higher level injuries.
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Journal of neurotrauma · Sep 2010
Comparative StudyAntagonism of R-type calcium channels significantly improves cerebral blood flow after subarachnoid hemorrhage in rats.
The effects of R-type calcium channels on cerebral blood flow (CBF) and vasospasm pathways following subarachnoid hemorrhage (SAH) have not been well studied. The aim of this study was to investigate the role of R-type calcium channels in vasospasm development and treatment. Sixty-five rats were randomly divided into four groups: sham (n = 14), SAH (n = 17), SAH + nimodipine (n = 17), and SAH + SNX-482 (n = 17). ⋯ Nimodipine had no significant effect on CBF reduction compared to the SAH group (p > 0.008), whereas SNX-482 significantly inhibited CBF reduction (p < 0.008). Both MLC2 phosphorylation and calponin degradation appeared to be inhibited by SNX-482, whereas the effects of nimodipine were relatively blunted. We concluded that an R-type calcium channel antagonist may improve CBF following SAH by partially inhibiting MLC2 phosphorylation and calponin degradation, and may exceed the potential of an L-type calcium channel antagonist, which suggests a more crucial role for R-type calcium channels in the development of SAH vasospasm and its treatment.