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Selective Neuronal Vulnerability to Oxidative Stress in the Brain
In this review, the currently known molecular and cellular factors that contribute to SNV to OS are summarized and include high intrinsic OS, high demand for ROS/RNS-based signaling, low ATP production, mitochondrial dysfunction, and high inflammatory response in vulnerable neurons. Expand
Molecular biology of glutamate receptors in the central nervous system and their role in excitotoxicity, oxidative stress and aging
  • E. Michaelis
  • Biology, Medicine
  • Progress in Neurobiology
  • 2 March 1998
A review of cascades of complex molecular events in the actions of L-glutamic acid as a neurotransmitter and its role in determining the physiological properties of glutamate receptors is presented. Expand
Direct measurement of glutamate release in the brain using a dual enzyme-based electrochemical sensor
An enzyme-based electrode with rapid response times and high degree of sensitivity and rapidity in responding to a rise in extracellular glutamate concentrations is described, which should make it now possible to measure the dynamic events associated with glutamate neurotransmission in the central nervous system. Expand
Basic FGF regulates the expression of a functional 71 kDa NMDA receptor protein that mediates calcium influx and neurotoxicity in hippocampal neurons
Data identify a mechanism whereby bFGF can modify neuronal responses to glutamate, and suggest that regulating the expression of excitatory amino acid receptors may provide a means for growth factors to influence the plasticity and degeneration of neural circuits. Expand
Transgenic Expression of Glud1 (Glutamate Dehydrogenase 1) in Neurons: In Vivo Model of Enhanced Glutamate Release, Altered Synaptic Plasticity, and Selective Neuronal Vulnerability
The Tg mice were significantly more resistant than wild-type mice to induction and duration of anesthesia produced by anesthetics that suppress Glu neurotransmission and might be a useful model for the effects of lifelong excess synaptic Glu release on CNS neurons and for age-associated neurodegenerative processes. Expand
Bioenergetic flux, mitochondrial mass and mitochondrial morphology dynamics in AD and MCI cybrid cell lines.
Reduced bioenergetic function is present during very early AD, is not brain-limited and induces protean retrograde responses that likely have both adaptive and mal-adaptive consequences. Expand
Oxidative inactivation of purified plasma membrane Ca2+-ATPase by hydrogen peroxide and protection by calmodulin.
In the present studies, inhibition of PMCA by H( 2)O(2) was characterized in enzyme purified from human erythrocyte membranes, indicating a CaM-induced conformational state resistant to oxidation. Expand
Genomic and biochemical approaches in the discovery of mechanisms for selective neuronal vulnerability to oxidative stress
Low energy reserves and high intrinsic stress levels are two underlying factors for neuronal selective vulnerability to OS and these mechanisms can be targeted in the future for the protection of vulnerable neurons. Expand
Anti-apoptotic protein Bcl-2 interacts with and destabilizes the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA).
The results suggest that the direct interaction of Bcl-2 with SERCA may be involved in the regulation of apoptotic processes in vivo through modulation of cytoplasmic and/or endoplasmic reticulum calcium levels required for the execution of apoptosis. Expand
High intrinsic oxidative stress may underlie selective vulnerability of the hippocampal CA1 region.
It was found that the CA1 region of hippocampus explants, cultured under normal conditions, had significantly higher superoxide levels and expressed both anti-oxidant genes and genes related to the generation of reactive oxygen species at significantly higher levels than the CA3. Expand