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Excitotoxic mechanisms in stroke: An update of concepts and treatment strategies
  • A. Hazell
  • Medicine, Biology
  • Neurochemistry International
  • 1 June 2007
TLDR
This review will focus on the latest advances in understanding of the excitotoxic process including the release of glutamate as a neurotransmitter and the potential contribution of complexins, the important role of astrocytes, and the role of glutamate uptake in white matter injury following ischemic insults. Expand
Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain injury
  • J. Yi, A. Hazell
  • Medicine, Biology
  • Neurochemistry International
  • 1 April 2006
TLDR
Evidence indicate glutamate transporters and splice variant are downregulated shortly following the insult, which then precipitates glutamate-mediated excitotoxic conditions, which should improve the likelihood of development of novel avenues for therapeutic intervention following TBI. Expand
Hepatic encephalopathy: An update of pathophysiologic mechanisms.
TLDR
The neural cell most vulnerable to liver failure is the astrocyte, and altered expression of several key proteins and enzymes including monoamine oxidase B, glutamine synthetase, and the so-called peripheral-type benzodiazepine receptors are modified. Expand
Update of cell damage mechanisms in thiamine deficiency: focus on oxidative stress, excitotoxicity and inflammation.
TLDR
Thiamine deficiency represents a model system with which to explore pathological mechanisms inherent in such maladies, with the potential to yield new insights into their possible treatment and prevention and their role in selective vulnerability in TD. Expand
Mechanisms of Neuronal Cell Death in Wernicke's Encephalopathy
TLDR
Evidence suggests that enzyme deficits result in focal lactic acidosis, cerebral energy impairment and depolarization resulting from increased release of glutamate in vulnerable brain structures, and it has been proposed that this depolarizing may result in N-Methyl-D-Aspartate receptor-mediated excitotoxicity as well as increased expression of immediate early genes resulting in apoptotic cell death. Expand
Manganese Neurotoxicity: An Update of Pathophysiologic Mechanisms
TLDR
Manganese causes a number of other functional changes in astrocytes including an impairment of glutamate transport, alterations of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase, production of nitric oxide, and increased densities of binding sites for the “peripheral-type” benzodiazepine receptor. Expand
Energy Metabolism in Astrocytes and Neurons Treated with Manganese: Relation among Cell-Specific Energy Failure, Glucose Metabolism, and Intercellular Trafficking Using Multinuclear NMR-Spectroscopic
TLDR
Changes in astrocytic metabolism may cause a loss of intercellular homeostatic equilibrium, contributing to neuronal dysfunction in manganese neurotoxicity. Expand
Brain energy metabolism in a sub-acute rat model of manganese neurotoxicity: an ex vivo nuclear magnetic resonance study using [1-13C]glucose.
TLDR
Ex vivo high-resolution NMR spectroscopy combined with in vivo injection of [1-13C]glucose was applied to gain insight into the mechanism(s) leading to energy failure in manganese neurotoxicity, providing new evidence in support of changes in brain energy metabolism playing an important role in mangsene neurotoxicity. Expand
Assessment of bioaccumulation, neuropathology, and neurobehavior following subchronic (90 days) inhalation in Sprague-Dawley rats exposed to manganese phosphate.
TLDR
The results reinforce the hypothesis that the olfactory bulb and caudate/putamen are the main brain tissues for Mn accumulation after subchronic inhalation exposure and confirm the need to investigate the exposure-response relationship of bioaccumulation, neuropathology, and neurobehavior following a sub chronic inhalations exposure to manganese phosphate. Expand
Effects of ammonia on glutamate transporter (GLAST) protein and mRNA in cultured rat cortical astrocytes
TLDR
The reduced capacity of astrocytes to reuptake glutamate following ammonia exposure may result in compromised neuron-astrocyte trafficking of glutamate and could contribute to the pathogenesis of the cerebral dysfunction characteristic of hyperammonemic syndromes such as hepatic encephalopathy. Expand
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