Journal of neurotrauma
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Journal of neurotrauma · Dec 2000
Riluzole reduces brain swelling and contusion volume in rats following controlled cortical impact injury.
Modulation of the glutamatergic and excitotoxic pathway may attenuate secondary damage following traumatic brain injury by reducing presynaptic glutamate release and blocking sodium channels in their inactivated state. The aim of the present study was to investigate the neuroprotective potential of riluzole in traumatic brain-injured rats. A left temporoparietal contusion was induced in 70 male Sprague-Dawley rats (controlled cortical impact injury). ⋯ Following trauma, CSF glutamate, taurine, and hypoxanthine levels were significantly increased compared to nontraumatized rats (p < 0.001). However, these neurochemical parameters as measured in cisternal CSF failed to reflect trauma-dependent increases in severity of tissue damage and did not reveal riluzole-mediated neuroprotection. Under the present study design, riluzole significantly reduced brain edema formation and contusion volume in rats subjected to a mild focal cortical contusion.
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Journal of neurotrauma · Dec 2000
Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury.
Traumatic brain injury is well known to cause deficits in learning and memory, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbances in forebrain cholinergic innervation which may contribute to such cognitive problems. This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after injury using the newly developed impact acceleration injury model. ⋯ Correlation analysis showed no relationship between synaptosomal choline uptake in any brain region and performance in either water maze learning or retention. This study shows that the impact acceleration model produces cognitive impairments equivalent to those seen with fluid percussion injury and controlled cortical impact. Compared with those models, the impact acceleration model does not produce a similar disruption of forebrain cholinergic nerve terminals.
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Journal of neurotrauma · Dec 2000
Rodent model of chronic central pain after spinal cord contusion injury and effects of gabapentin.
Spinal cord injury (SCI) often results in abnormal pain syndromes in patients. We present a recently developed SCI mammalian model of chronic central pain in which the spinal cord is contused at T8 using the NYU impactor device (10-g rod, 2.0-mm diameter, 12.5-mm drop height), an injury which is characterized behaviorally as moderate. Recovery of locomotor function was assessed with an open field test and scored using the open field test scale (BBB scale). ⋯ To demonstrate the validity of this model as a central pain model, gabapentin, an agent used clinically for central pain, was given i.p. at 10 or 30 mg/kg. Gabapentin treatment significantly and reversibly changed the responses, consistent with the attenuation of the abnormal sensory behavior, and the attenuated responses lasted for the duration of the drug effect (up to 6 h). These results support the use of the spinal contusion model in the study of chronic central pain after SCI.
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Journal of neurotrauma · Dec 2000
Comparative StudyIsoflurane improves long-term neurologic outcome versus fentanyl after traumatic brain injury in rats.
Despite routine use of fentanyl in patients after traumatic brain injury (TBI), it is unclear if it is the optimal sedative/analgesic agent. Isoflurane is commonly used in experimental TBI. We hypothesized that isoflurane would be neuroprotective versus fentanyl after TBI. ⋯ Alternatively, fentanyl may be detrimental. Isoflurane may mask beneficial effects of novel agents tested in TBI models. Additionally, fentanyl may not be optimal early after TBI in humans.