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Assessing mitochondrial dysfunction in cells
Measurement of both respiration and potential during appropriate titrations enables the identification of the primary sites of effectors and the distribution of control, allowing deeper quantitative analyses, as discussed in the present review.
Mitochondria and neuronal survival.
The functional bioenergetics of isolated mitochondria are reviewed, with emphasis on the chemiosmotic proton circuit and the application (and occasional misapplication) of these principles to intact neurons.
Thermogenic mechanisms in brown fat.
Mitochondrial membrane potential and neuronal glutamate excitotoxicity: mortality and millivolts
Monitoring of the major component of Deltap, the mitochondrial membrane potential Deltapsim, in intact neurones exposed to excitotoxic stimuli, in the hope of establishing the causal relationships between cell death and mitochondrial dysfunction.
Calcium‐Dependent and‐Independent Release of Glutamate from Synaptosomes Monitored by Continuous Fluorometry
An enzyme‐linked fluorometric assay is described for the continuous monitoring of the unidirectional efflux of glutamate from guinea‐pig synaptosomes, consistent with an intrasynaptosomal relocation of the amino acid.
The release and uptake of excitatory amino acids.
The contrasting pharmacology and ionic dependence of the glutamate uptake carriers in the vesicle membrane and in the plasma membrane explain how glutamate (but probably not aspartate) can function as a neurotransmitter, and why the extracellular glutamate concentration rises to neurotoxic levels in brain anoxia.
The Relationship between Free and Total Calcium Concentrations in the Matrix of Liver and Brain Mitochondria*
Three sequential phases of mitochondrial calcium accumulation can be distinguished: matrix dehydrogenase regulation, buffering of extramitochondrial free calcium, and finally activation of the permeability transition, which is investigated in rat liver and brain mitochondria.
Calpain I Induces Cleavage and Release of Apoptosis-inducing Factor from Isolated Mitochondria*
A novel mechanism of AIF release involving calpain processing is defined and a potential molecular checkpoint for cytoprotective interventions is identified that is identified in vivo following acute rodent brain injuries.
Mitochondrial Membrane Potential and Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells
It is concluded that transient Ca2+loading of mitochondria as a consequence of NMDA receptor activation initiates oxidative damage to both plasma membrane Ca 2+ extrusion pathways and the inhibition of mitochondrial respiration.