Articles: brain-injuries.
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Although glucose is the main carbohydrate energy substrate for the normal brain, several studies published over the last 10 years now challenge this assumption. The activated brain increases its metabolism to meet increased energy demands by glycolysis after injury. In vitro studies now show that lactate alone can serve as an energy source to maintain synaptic function. ⋯ After 30 min, the brain was removed, frozen, and cut into 20 microm sections for autoradiography. Uptake of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain also took up the 14C-label. This increased concentration of radioactive lactate at the injury site suggests that the injured brain may use the lactate as an energy source.
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Traumatic brain injury (TBI) can produce chronic cognitive learning/memory deficits that are thought to be mediated, in part, by impaired hippocampal function. Experimentally induced TBI is associated with deficits in hippocampal synaptic plasticity (long-term potentiation, or LTP) at acute post-injury intervals but plasticity has not been examined at long-term survival periods. The present study was conducted to assess the temporal profile of LTP after injury and to evaluate the effects of injury severity on plasticity. ⋯ These experiments reveal a previously unknown effect of TBI whereby experimentally induced injury results in a chronic inability of the CA1 hippocampus to maintain synaptic plasticity. They also provide evidence that sham surgical procedures can significantly influence hippocampal physiology at the acute post-TBI intervals. The results have implications for the mechanisms underlying the impaired synaptic plasticity following TBI.
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J. Cereb. Blood Flow Metab. · Apr 2000
Expression of Fas and Fas ligand after experimental traumatic brain injury in the rat.
Apoptotic cell death plays an important role in the cascade of neuronal degeneration after traumatic brain injury (TBI), but the underlying mechanisms are not fully understood. However, increasing evidence suggests that expression of Fas and its ligand (FasL) could play a major role in mediating apoptotic cell death in acute and chronic neurologic disorders. To further investigate the temporal pattern of Fas and FasL expression after experimental TBI in the rat, male Sprague Dawley rats were subjected to unilateral cortical impact injury. ⋯ These results reveal induction of Fas and FasL expression in the cortex after TBI in the rat. Further, these data implicate an involvement of Fas and FasL in the pathophysiologic mechanism of apoptotic neurodegeneration after TBI. Last, these data suggest that strategies aimed to repress posttraumatic Fas- and FasL-induced apoptosis may open new perspectives for the treatment of TBI.
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Curr. Opin. Pediatr. · Apr 2000
ReviewCerebral hypothermia for prevention of brain injury following perinatal asphyxia.
The possibility that hypothermia has a therapeutic role during or after resuscitation from severe perinatal asphyxia has been a longstanding focus of research. Early studies using short periods of cooling had limited and contradictory results. ⋯ These encouraging results must be balanced against the well-known adverse systemic effects of hypothermia. Randomized clinical trials are in progress to test the safety and efficacy of cerebral hypothermia.