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Uncoupling protein-2 prevents neuronal death and diminishes brain dysfunction after stroke and brain trauma
Whereas uncoupling protein 1 (UCP-1) is clearly involved in thermogenesis, the role of UCP-2 is less clear. Using hybridization, cloning techniques and cDNA array analysis to identify inducibleExpand
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Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
ABSTRACT— A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial bloodExpand
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Cyclosporin A, But Not FK 506, Protects Mitochondria and Neurons against Hypoglycemic Damage and Implicates the Mitochondrial Permeability Transition in Cell Death
Induction of the mitochondrial permeability transition (MPT) has been implicated in cellular apoptosis and in ischemia–reperfusion injury. During MPT, a channel in the inner mitochondrial membrane,Expand
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Mechanisms of neural plasticity following brain injury
Brain insults cause rapid cell death, and a disruption of functional circuits, in the affected regions. As the injured tissue recovers from events associated with cell death, regenerative processesExpand
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Structural and Functional Damage Sustained by Mitochondria after Traumatic Brain Injury in the Rat: Evidence for Differentially Sensitive Populations in the Cortex and Hippocampus
The cellular and molecular pathways initiated by traumatic brain injury (TBI) may compromise the function and structural integrity of mitochondria, thereby contributing to cerebral metabolicExpand
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Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist.
  • T. Wieloch
  • Chemistry, Medicine
  • Science
  • 8 November 1985
The possibility that neuronal damage due to hypoglycemia is induced by agonists acting on the N-methyl-D-aspartate (NMDA) receptor was investigated in the rat caudate nucleus. Local injections of anExpand
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Mitochondrial permeability transition in acute neurodegeneration.
Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinicalExpand
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The distribution of hypoglycemic brain damage
SummaryRats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose, they were allowed to wake up andExpand
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Mitochondrial damage and dysfunction in traumatic brain injury.
The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observedExpand
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Flow cytometric analysis of mitochondria from CA1 and CA3 regions of rat hippocampus reveals differences in permeability transition pore activation
Mitochondria are important in the pathophysiology of several neurodegenerative diseases, and mitochondrial production of reactive oxygen species (ROS), membrane depolarization, permeability changesExpand
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