David G. Nicholls

Mitochondrial function and dysfunction in the cell: its relevance to aging and aging-related disease.

Barbiturates induce mitochondrial depolarization and potentiate excitotoxic neuronal death.

The relationship between free and total calcium concentrations in the matrix of liver and brain mitochondria.

Interactions between mitochondrial bioenergetics and cytoplasmic calcium in cultured cerebellar granule cells.

Oxidative alpha-ketoglutarate dehydrogenase inhibition via subtle elevations in monoamine oxidase B levels results in loss of spare respiratory capacity: implications for Parkinson's disease.

Bioenergetics and transmitter release in the isolated nerve terminal.

Mitochondrial membrane potential and aging.

In situ respiration and bioenergetic status of mitochondria in primary cerebellar granule neuronal cultures exposed continuously to glutamate.

Relationships between superoxide levels and delayed calcium deregulation in cultured cerebellar granule cells exposed continuously to glutamate.

The integration of mitochondrial calcium transport and storage.

Calpain I induces cleavage and release of apoptosis-inducing factor from isolated mitochondria.

Mitochondria and calcium signaling.

Acute glutathione depletion restricts mitochondrial ATP export in cerebellar granule neurons.

Commentary on: 'old and new data, new issues: the mitochondrial Deltapsi' by H. Tedeschi.

Simultaneous monitoring of ionophore- and inhibitor-mediated plasma and mitochondrial membrane potential changes in cultured neurons.

The physiological regulation of uncoupling proteins.

Mitochondrial-dependent Ca2+ handling in Huntington's disease striatal cells: effect of histone deacetylase inhibitors.

Mitochondrial dysfunction in Huntington's disease: the bioenergetics of isolated and in situ mitochondria from transgenic mice.

Bioenergetics of mitochondria in cultured neurons and their role in glutamate excitotoxicity.

Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone.

Mitochondrial and plasma membrane potential of cultured cerebellar neurons during glutamate-induced necrosis, apoptosis, and tolerance.

Inducible alterations of glutathione levels in adult dopaminergic midbrain neurons result in nigrostriatal degeneration.

Experimental assessment of bioenergetic differences caused by the common European mitochondrial DNA haplogroups H and T.

MAO-B elevation in mouse brain astrocytes results in Parkinson's pathology.

Forty years of Mitchell's proton circuit: From little grey books to little grey cells.

Effects of neuroglobin overexpression on mitochondrial function and oxidative stress following hypoxia/reoxygenation in cultured neurons.

Measurement of instantaneous velocity vectors of organelle transport: mitochondrial transport and bioenergetics in hippocampal neurons.

UCPs--unlikely calcium porters.

Oxidative stress and energy crises in neuronal dysfunction.

Reactive oxygen species regulation by AIF- and complex I-depleted brain mitochondria.

Mitochondrial calcium function and dysfunction in the central nervous system.

Real-time visualization of cytoplasmic calpain activation and calcium deregulation in acute glutamate excitotoxicity.

Bioenergetic analysis of isolated cerebrocortical nerve terminals on a microgram scale: spare respiratory capacity and stochastic mitochondrial failure.

Metabolic control analysis in a cellular model of elevated MAO-B: relevance to Parkinson's disease.

Quantitative microplate-based respirometry with correction for oxygen diffusion.

Tight coupling between glucose and mitochondrial metabolism in clonal beta-cells is required for robust insulin secretion.

Spare respiratory capacity, oxidative stress and excitotoxicity.

Stochastic aspects of transmitter release and bioenergetic dysfunction in isolated nerve terminals.

Mitochondrial ion circuits.

Intrinsic bioenergetic properties and stress sensitivity of dopaminergic synaptosomes.

Assessing mitochondrial dysfunction in cells.

Fluorescence measurement of mitochondrial membrane potential changes in cultured cells.