Journal of neurotrauma
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Journal of neurotrauma · Dec 2002
Comparative StudyAlcohol consumption in traumatic brain injury: attenuation of TBI-induced hyperthermia and neurocognitive deficits.
Clinical and animal studies indicate that hyperthermia during or after traumatic brain injury (TBI) is associated with poor outcome. Alcohol intoxication, a complicating risk factor in many cases of head injury, has been found to both worsen or attenuate posttraumatic neural damage and outcome. The purpose of the present study was to determine whether chronic ethanol consumption would affect TBI-induced hyperthermia and deficits in spatial learning. ⋯ When tested at 3-4 weeks after TBI, E-E rats required significantly fewer trials than E-P rats to reach criterion in the Morris water maze. In sum, continuous consumption of ethanol before and after TBI attenuated TBI-induced hyperthermia and deficits in spatial learning. Whereas the results suggest that this ethanol regimen may be neuroprotective, a causal relationship between the two outcomes remains to be determined.
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Journal of neurotrauma · Dec 2002
Comparative StudyNeutralizing intraspinal nerve growth factor with a trkA-IgG fusion protein blocks the development of autonomic dysreflexia in a clip-compression model of spinal cord injury.
Increased intraspinal nerve growth factor (NGF) after spinal cord injury (SCI) is detrimental to the autonomic nervous system. Autonomic dysreflexia is a debilitating condition characterized by episodic hypertension, intense headache, and sweating. Experimentally, it is associated with aberrant primary afferent sprouting in the dorsal horn that is nerve growth factor (NGF)-dependent. ⋯ Likewise, the MAP response to cutaneous stimulation was also reduced in rats treated with trkA-IgG (20 +/- 1 vs. 29 +/- 2). In contrast, trkA-IgG treatment had no effect on heart rate responses during colon distension or cutaneous stimulation. These results indicate that treatment with trkA-IgG to block NGF suppresses the development of autonomic dysreflexia after a clinically relevant spinal cord injury.
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Journal of neurotrauma · Dec 2002
Comparative StudyTemporal and spatial profile of phosphorylated mitogen-activated protein kinase pathways after lateral fluid percussion injury in the cortex of the rat brain.
Mitogen-activated protein kinases (MAPK) play a crucial role in signal transduction that regulates gene expression through transcriptional factor activity. The purpose of this study was to investigate the temporal expression and topographic distribution of the activated MAPK pathways including extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 MAPK following traumatic brain injury (TBI) in the cortex of the rat brain. Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury of moderate severity (3.5-4.0 atm) using the Dragonfly device model (no. ⋯ The immunoreactivity for p-ERK was confirmed up until 30 min after TBI in the superficial neuronal layers. Double immunostaining using a glial-specific marker demonstrated that p-ERK was prominent in astrocytes 6 h after TBI. The current results suggest that the ERK and JNK pathways, but not the p38 MAPK pathways are involved in signal transduction in the cortex following TBI.
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Journal of neurotrauma · Nov 2002
Comparative StudyInfluence of norepinephrine and dopamine on cortical perfusion, EEG activity, extracellular glutamate, and brain edema in rats after controlled cortical impact injury.
Following traumatic brain injury, catecholamines given to ameliorate cerebral perfusion may induce brain damage via cerebral arteriolar constriction and increased neuronal excitation. In the present study the acute effects of norepinephrine and dopamine on pericontusional cortical perfusion (rCBF), electroencephalographic (EEG) activity, extracellular glutamate, and brain edema were investigated in rats following controlled cortical impact injury (CCI). rCBF, cerebral perfusion pressure (CPP), EEG activity, and glutamate were determined before, during, and after infusing norepinephrine or dopamine, increasing MABP to 120 mm Hg for 90 min at 4 h after CCI. Control rats received physiological saline. ⋯ Despite significantly increasing MABP and CPP to the same extent, norepinephrine and dopamine seem to differentially influence pericontusional cortical perfusion and glutamatergic transmission. In addition to the pressure-passive increase in CPP local cerebral effects seem to account for the sustained norepinephrine-induced increase in pericontusional cortical perfusion. The significantly elevated pericontusional glutamate concentrations in conjunction with the increased EEG activity suggest a sustained metabolically driven increase in cortical perfusion during norepinephrine infusion.
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Journal of neurotrauma · Oct 2002
ReviewRoller coasters, g forces, and brain trauma: on the wrong track?
There has been enormous attention in the general press on the possibility that high G force roller coasters are inducing brain injury in riders. Armed with a handful of anecdotal case reports of brain injuries, the U. S. ⋯ With this model, we calculated peak head rotational accelerations in three directions. Even for a conservative worst-case scenario, we found that the highest estimated peak head accelerations induced by roller coasters were far below conventional levels that are predicted for head injuries. Accordingly, our findings do not support the contention that current roller coaster rides produce high enough forces to mechanically deform and injure the brain.