Spare respiratory capacity, oxidative stress and excitotoxicity.

David G. Nicholls

@article{Nicholls2009SpareRC, title={Spare respiratory capacity, oxidative stress and excitotoxicity.}, author={David G. Nicholls}, journal={Biochemical Society transactions}, year={2009}, volume={37 Pt 6}, pages={1385-8} }

David G. Nicholls

Published 2009 in Biochemical Society transactions

DOI:10.1042/BST0371385

Chronic exposure to glutamate (glutamate excitotoxicity) exacerbates neuronal damage in the aftermath of stroke and is implicated in a variety of neurodegenerative disorders. Mitochondria play a central role in the survival or death of the exposed neuron. Calcium, oxidative stress and ATP insufficiency play closely interlocked roles that may be investigated with primary neuronal cultures.

A. V. Wabnitz, T. P. Storozhevykh, Y. E. Senilova, V. G. Pinelis, B. I. Khodorov
Biol . Membr .
2006

A. V. Wabnitz, T. P. Storozhevykh, Y. E. Senilova, V. G. Pinelis, B. I. Khodorov
neurons. Biol. Membr
2006

Spare respiratory capacity, oxidative stress and excitotoxicity.

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References

Publications referenced by this paper.

Mild mitochondrial uncoupling in mice affects energy metabolism, redox balance and longevity.

'Mild Uncoupling' does not decrease mitochondrial superoxide levels in cultured cerebellar granule neurons but decreases spare respiratory capacity and increases toxicity to glutamate and oxidative stress.

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

Uncoupling is without an effect on the production of reactive oxygen species by in situ synaptic mitochondria.

The mitochondrial permeability transition from in vitro artifact to disease target.

The permeability transition pore is not a prerequisite for glutamate - induced calcium deregulation and mitochondrial depolarization in brain neurons

The permeability transition pore is not a prerequisite for glutamate-induced calcium deregulation and mitochondrial depolarization in brain

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

Excitotoxic calcium overload in a subpopulation of mitochondria triggers delayed death in hippocampal neurons.

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

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