Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
Primary blast exposure increases hippocampal vulnerability to subsequent exposure reducing long-term potentiation.
Up to 80% of injuries sustained by U. S. soldiers in Operation Enduring Freedom and Operation Iraqi Freedom were the result of blast exposure from improvised explosive devices. Some soldiers experience multiple blasts while on duty, and it has been suggested that symptoms of repetitive blast are similar to those that follow multiple non-blast concussions, such as sport-related concussion. ⋯ The repeated blast exposure with a 24 h interval increased microglia staining and activation significantly but did not significantly increase cell death or damage axons, dendrites, or principal cell layers. Lack of overt structural damage and change in basal stimulated neuron response suggest that injury from repetitive primary blast exposure may specifically affect long-term potentiation. Our studies suggest repetitive primary blasts can exacerbate injury dependent on the injury severity and interval between exposures.
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Journal of neurotrauma · Oct 2016
White matter injury susceptibility via fiber strain evaluation using whole-brain tractography.
Microscale brain injury studies suggest axonal elongation as a potential mechanism for diffuse axonal injury (DAI). Recent studies have begun to incorporate white matter (WM) structural anisotropy in injury analysis, with initial evidence suggesting improved injury prediction performance. In this study, we further develop a tractography-based approach to analyze fiber strains along the entire lengths of fibers from voxel- or anatomically constrained whole-brain tractography. ⋯ As an illustration, we evaluate the DAI susceptibilities of WM voxels and transcallosal fiber tracts in three idealized head impacts. Findings suggest the potential importance of the tractography-based approach for injury prediction. These efforts may enable future studies to correlate WM mechanical responses with neuroimaging, cognitive alteration, and concussion, and to reveal the relative vulnerabilities of neural pathways and identify the most vulnerable ones in real-world head impacts.
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Journal of neurotrauma · Oct 2016
Underlying Cortical Dysplasia as Risk Factor for Traumatic Epilepsy: An Animal Study.
Traumatic brain injury (TBI) is a significant risk factor for development of epilepsy in humans. It is unclear, however, why some persons are at an increased risk of becoming epileptic, while others recover from the TBI seizure-free. We previously showed that the presence of a proepileptic pathology increases the risk of epilepsy in an animal model of cortical dysplasia (CD) after a secondary insult, which we described as the "second hit". ⋯ All of the CD animals exhibited interictal spiking after TBI, while only a portion of nondysplastic animals produced spikes. These results suggest that the presence of a proepileptic pathology may increase the risk for the development of epilepsy after TBI. Diagnosis and treatment of TBI may depend on underlying pathologies contributing to epilepsy after a brain injury.
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Journal of neurotrauma · Oct 2016
Minimal traumatic brain injury in mice - PAR-1 and thrombin related changes.
Minimal traumatic brain injury (mTBI) is partially defined by the existence of retrograde amnesia and is associated with microscopic bleeds containing activated coagulation factors. In a previous study, we have found that mTBI immediately releases thrombin-like activity in the brain, which induces amnesia by activating protease-activated receptor 1 (PAR-1) and blocking long-term potentiation (LTP). In the present study, we assessed the effects of mTBI on thrombin and PAR-1 levels in the brain using the same model. ⋯ Interestingly, the late elevation in thrombin-like activity was also associated with elevation of the major central nervous system thrombin inhibitor, protease nexin-1, 72 h post-mTBI (10%; p < 0.005). When thrombin was injected into brain ventricles, an increased sensitivity to seizure-like activity was detected at 72 h post-mTBI. The results are compatible with astrocyte activation post-mTBI resulting in increased thrombin secretion, PAR-1 expression, and seizure sensitivity.
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Journal of neurotrauma · Oct 2016
Minor Functional Deficits in Basic Response Patterns for Reinforcement following Frontal Traumatic Brain Injury in Rats.
Traumatic brain injury (TBI) is a major contributor to numerous psychiatric conditions and chronic behavioral dysfunction. Recent studies in experimental brain injury have begun to adopt operant methodologies to assess these deficits, all of which rely on the process of reinforcement. No studies have directly examined how reinforced behaviors are affected by TBI, however. ⋯ Further, injured rats were specifically impaired at lower response requirements on the progressive ratio. Taken together, these findings indicate that simple reinforced behaviors are mostly unaffected after TBI, except in the case of variable ratio schedules, but the altered performance on the higher-order progressive ratio schedule suggests changes involving motivation or potentially perseveration. These findings validate operant measures of more complex behaviors for brain injury, all of which rely on reinforcement and can be taken into consideration when adapting and developing novel functional assessments.