Journal of neurotrauma
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Journal of neurotrauma · Feb 2006
Mechanisms and consequences of neuronal stretch injury in vitro differ with the model of trauma.
The deformation to the brain that occurs during traumatic brain injury (TBI) results in a complex strain distribution throughout the brain tissue. Recently, many in vitro models of neuronal injury have been developed to simplify the mechanics which occur during TBI. We hypothesized that the type of mechanical insult imparted onto neurons would significantly alter both the mechanism and severity of the neuronal response to injury. ⋯ Despite the large ([Ca2+]i) transients, neither injury profile resulted in death within 24 h of injury. Interestingly, though, uniaxially stretched neurons exhibited enhanced [Ca+2]i influx following NMDA stimulation 24 h after trauma, compared to both control and biaxially stretched neurons. These data point out that the type of mechanical insult will influence the acute mechanisms of injury in vitro, can cause differences in the response to potential secondary excitotoxic injury mechanisms, and emphasizes the need to further study how these mechanical conditions can separately affect cell fate following mechanical injury.
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Journal of neurotrauma · Feb 2006
Correlation between target reinnervation and distribution of motor axons in the injured rat sciatic nerve.
Peripheral nerve injuries are rarely followed by complete return of function. Deficits are particularly important for motor function, resulting in paralysis and muscle atrophy. In different groups, the sciatic nerve was either crushed or transected and repaired by direct suture or by tube repair using silicone or collagen tubes. ⋯ The normal fascicular architecture and grouping of ChAT+ fibers were maintained after nerve crush, but lost after section and repair, where motor fibers were scattered within small regenerated fascicles throughout the nerve. The loss of fascicular organization was related to the deficient recovery of locomotor function. Thus, labeling of motor axons by ChAT immunohistochemistry provides useful information for the study of the degree and specificity of nerve regeneration.
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Journal of neurotrauma · Jan 2006
Early, transient increase in complexin I and complexin II in the cerebral cortex following traumatic brain injury is attenuated by N-acetylcysteine.
Alteration of excitatory neurotransmission is a key feature of traumatic brain injury (TBI) in which extracellular glutamate levels rise. Although increased synaptic release of glutamate occurs at the injury site, the precise mechanism is unclear. Complexin I and complexin II constitute a family of cytosolic proteins involved in the regulation of neurotransmitter release, competing with the chaperone protein alpha-SNAP (soluble N-ethylmaleimide-sensitive factor-attachment protein) for binding to the synaptic vesicle protein synaptobrevin as well as the synaptic membrane proteins SNAP-25 and syntaxin, which together form the SNAP receptor (SNARE) complex. ⋯ Neuronal loss was also reduced in the injured hemisphere with post-TBI NAC treatment. Our findings suggest a dysregulation of both inhibitory and excitatory neurotransmission following traumatic injury that is responsive to antioxidant treatment. These alterations in complexin levels may also play an important role in neuronal cell loss following TBI, and thus contribute to the pathophysiology of cerebral damage following brain injury.
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Journal of neurotrauma · Jan 2006
Behavioral and histological characterization of unilateral cervical spinal cord contusion injury in rats.
Most experimental studies of spinal cord injury (SCI) in rats damage the thoracic cord, with the consequent functional loss being due to interruption of long tracts connecting the caudal spinal cord to the rostral nervous system. Less work has been done evaluating injury to the cervical cord, even though it is the most common level of human SCI. In addition to the long tracts, the cervical spinal cord contains the sensory and motor neurons responsible for upper extremity function. ⋯ Compared to controls, animals receiving SCI exhibited injury severity-specific deficits in forelimb, locomotor, and hindlimb function persisting for 6-weeks post-SCI. Histological analysis revealed ipsilateral containment of the injury, and differentiation between groups on all measures except motor neuron counts. This model has many advantages: (1) minimal animal care requirements post-SCI, (2) within subject controls, (3) functional loss involves primarily the ipsilateral forelimb, and (4) it is a behavioral and histological model for both gray and white matter damage caused by contusive SCI.
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Journal of neurotrauma · Jan 2006
Comparative StudyComparison of seven anesthetic agents on outcome after experimental traumatic brain injury in adult, male rats.
Isoflurane is commonly used in experimental traumatic brain injury (TBI), both before and early after injury, yet it is rarely used clinically. Narcotics and benzodiazepines are frequently used after injury in clinical TBI. We compared seven anesthetic/sedative agents applied after injury in the controlled cortical impact model: diazepam, fentanyl, isoflurane, ketamine, morphine, pentobarbital, and propofol. ⋯ Our data support beneficial effects of isoflurane early after experimental TBI. Our data suggest that the early post-TBI use of isoflurane, despite practical logistical issues, could potentially provide clinical benefits in TBI--versus other commonly used sedatives or analgesics. Furthermore, the choice of post-injury sedation and analgesia could have important implications on attempts to translate novel therapies from bench to field or bedside.