Journal of neurotrauma
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Journal of neurotrauma · Dec 1994
Combined fluid percussion brain injury and entorhinal cortical lesion: a model for assessing the interaction between neuroexcitation and deafferentation.
Laboratory studies suggest that excessive neuroexcitation and deafferentation contribute to long-term morbidity following human head injury. Because no current animal model of traumatic brain injury (TBI) has been shown to combine excessive neuroexcitation and significant levels of deafferentation, we developed a rat model combining the neuroexcitation of fluid percussion TBI with subsequent entorhinal cortical (EC) deafferentation. In this paradigm, moderate fluid percussion TBI was induced in each rat, followed 24 h later by bilateral EC lesion (BEC). ⋯ Specifically, the laminar pattern of presynaptic rearrangement induced by BEC lesion did not occur after TBEC injury. The present results show that axonal injury and its attendant deafferentation, when coupled with traumatically induced neuroexcitation, produce an enhancement of the morbidity associated with TBI. Moreover, they indicate that this model can effectively be used to study the interaction between neuroexcitation and synaptic plasticity.
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Journal of neurotrauma · Dec 1994
Widespread metabolic depression and reduced somatosensory circuit activation following traumatic brain injury in rats.
The effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. ⋯ Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.
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Electric currents of small magnitude have been used successfully to induce regrowth of injured spinal cord fibers. The purpose of this study was to determine the potentials and current density distributions on the surface, as well as within the spinal cord, after the application of exogenous electric fields. A 10 microA DC current was applied epidurally to the spinal cord using two different electrode configurations. ⋯ The current density was more localized on the dorsal surface of the spinal cord for the D-D configuration. In contrast, in the V-D configuration, the current density was greater near the anode on the ventral surface and near the cathode on the dorsal surface of the spinal cord. As a result of the anode being located ventrally, there was a more uniform current density distribution within the spinal cord.
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Journal of neurotrauma · Oct 1994
Neurofilament 68 and neurofilament 200 protein levels decrease after traumatic brain injury.
We have examined the effect of lateral cortical impact injury on the levels of axonal cytoskeletal proteins in adult rats. Traumatic brain injury (TBI) causes a significant decrease in the protein levels of two prominent neurofilament (NF) proteins, NF68 and NF200. We employed quantitative immunoreactivity measurements on Western blots to examine NF68 and NF200 levels in homogenates of hippocampal and cortical tissue taken at several intervals postinjury. ⋯ This NF68 antigenicity pattern suggests the production of NF68 breakdown products caused by the pathologic activation of neuronal proteases, such as calpain. Putative NF68 breakdown products increase significantly until 1 day postinjury, suggesting that NF degradation may be ongoing until that time and indicating that a potential therapeutic window may exist within the first 24 h postinjury. In summary, these data identify specific biochemical alterations of the neuronal cytoskeleton following TBI and lay a foundation for further investigation of postinjury cytoskeletal changes in neuronal processes.