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
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.
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Journal of neurotrauma · Apr 2012
Morphological alteration and reduction of MAP2-immunoreactivity in pyramidal neurons of cerebral cortex in a rat model of focal cortical compression.
Subdural hematoma causes cortical damage including brain tissue disruption, often resulting in neuronal dysfunction and neurological impairment. The aim of the present study was to identify the relationship between cerebral compression and neuronal injury. In this report, we investigated time-dependent morphological alterations within layers II, III, and V pyramidal neurons in the cerebral cortex, using Golgi-Cox staining and immunohistochemistry for microtubule-associated protein 2 (MAP2) in a rat model of focal cortical compression. ⋯ The number of MAP2-immunoreactive neurons was significantly decreased at 12 h compared with the contralateral cerebral cortex in the same animal. Dendritic changes in layers II, III, and V pyramidal neurons were accompanied by reductions in intracellular MAP2-immunoreactive materials. The present results suggest that cortical compression causes alteration of cellular morphology as a consequence of injury, and that these morphological changes may be related to reductions in MAP2-immunoreactive materials.