Journal of neurotrauma
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Journal of neurotrauma · Apr 2012
Apoptotic cascades in the central auditory pathway after noise exposure.
Noise exposure leads to dramatic physiological and anatomical changes within the central auditory pathway in addition to the well-known cochlear damage. Our group previously described a significant loss of neurons in different central auditory structures upon acoustic overstimulation. The aim of the present study was to investigate if declined neuronal cell density is caused by apoptotic mechanisms. ⋯ In the VCN, the number of TUNEL-positive cells of the same grid size was three times the numbers in the ICC. Our results show that noise exposure induces apoptosis-related pathophysiological changes within the central auditory pathway in a time-dependent manner. This may represent potential therapeutic targets, and helps clarify the complex psychoacoustic phenomena of noise-induced hearing loss.
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Journal of neurotrauma · Apr 2012
Disruptions in the regulation of extracellular glutamate by neurons and glia in the rat striatum two days after diffuse brain injury.
Disrupted regulation of extracellular glutamate in the central nervous system contributes to and can exacerbate the acute pathophysiology of traumatic brain injury (TBI). Previously, we reported increased extracellular glutamate in the striatum of anesthetized rats 2 days after diffuse brain injury. To determine the mechanism(s) responsible for increased extracellular glutamate, we used enzyme-based microelectrode arrays (MEAs) coupled with specific pharmacological agents targeted at in vivo neuronal and glial regulation of extracellular glutamate. ⋯ Furthermore, glutamate clearance measured by locally applying glutamate into the extracellular space revealed significant reductions in glutamate clearance parameters in brain-injured animals compared with sham. Taken together, these data indicate that disruptions in calcium-mediated glutamate release and glial regulation of extracellular glutamate contribute to increased extracellular glutamate in the striatum 2 days after diffuse brain injury. Overall, these data suggest that therapeutic strategies used to regulate glutamate release and uptake may improve excitatory circuit function and, possibly, outcomes following TBI.
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Journal of neurotrauma · Apr 2012
Post-traumatic hypoxia exacerbates neuronal cell death in the hippocampus.
Hypoxia frequently occurs in patients with traumatic brain injury (TBI) and is associated with increased morbidity and mortality. This study examined the effects of immediate or delayed post-traumatic hypoxia (fraction of inspired oxygen [FiO(2)] 11%) on acute neuronal degeneration and long-term neuronal survival in hippocampal fields after moderate fluid percussion injury in rats. In Experiment 1, hypoxia was induced for 15 or 30 min alone or immediately following TBI. ⋯ In Experiment 3, 30 min of immediate hypoxia significantly reduced the numbers of surviving neurons in the CA3 at 14 days after TBI. The greatly increased vulnerability in all hippocampal fields by immediate 30 min post-traumatic hypoxia provides a relevant model of TBI complicated with hypoxia/hypotension. These data underscore the significance of the secondary insult, the necessity to better characterize the range of injuries experienced by the TBI patient, and the importance of strictly avoiding hypoxia in the early management of TBI patients.
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Journal of neurotrauma · Apr 2012
Challenging the role of adaptive immunity in neurotrauma: Rag1(-/-) mice lacking mature B and T cells do not show neuroprotection after closed head injury.
The role of adaptive immunity in contributing to post-traumatic neuroinflammation and neuropathology after head injury remains largely unexplored. The present study was designed to investigate the pathophysiological sequelae of closed head injury in Rag1(-/-) mice devoid of mature B and T lymphocytes. C57BL/6 wild-type and Rag1(-/-) mice were subjected to experimental closed head injury, using a standardized weight-drop device. ⋯ In contrast, the levels of pro- and anti-inflammatory cytokines and pro-apoptotic and anti-apoptotic mediators remained in a similar range for both groups, and the histological analysis of brain sections did not reveal a difference in reactive astrogliosis, tissue destruction, and neuronal cell death in Rag1(-/-) compared to wild-type mice. These findings suggest that adaptive immunity is not of crucial importance for initiating and sustaining the inflammatory neuropathology after closed head injury. The attenuated extent of post-traumatic complement activation seen in Rag1(-/-) mice implies a cross-talk between innate and adaptive immune responses, which requires further investigation in future studies.
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Journal of neurotrauma · Apr 2012
Cranioplasty after decompressive craniectomy: the effect of timing on postoperative complications.
Decompressive craniectomy (DC) due to intractably elevated intracranial pressure mandates later cranioplasty (CP). However, the optimal timing of CP remains controversial. We therefore analyzed our prospectively conducted database concerning the timing of CP and associated post-operative complications. ⋯ We provide detailed data on surgical timing and complications for cranioplasty after DC. The present data suggest that patients who undergo late CP might benefit from a lower complication rate. This might influence future surgical decision making regarding optimal timing of cranioplasty.