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Three-dimensional Imaging and Analysis of Mitochondria within Human Intraepidermal Nerve Fibers

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Calcium-dependent mitochondrial function and dysfunction in neurons.

Natalia B Pivovarova¹, S Brian Andrews

¹Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-4477, USA.

The FEBS Journal

|July 28, 2010

Summary

This summary is machine-generated.

Mitochondria manage cellular calcium, influencing responses from gene transcription to cell death. This review explores mitochondrial calcium handling, its role in neurotoxicity, and its connection to reactive oxygen species.

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Area of Science:

Neuroscience
Cell Biology
Biochemistry

Background:

Calcium ions are crucial signaling molecules in cellular responses.
Mitochondria play a key role in regulating intracellular calcium levels in neurons.
Dysfunctional mitochondrial calcium handling is implicated in neurodegenerative diseases.

Purpose of the Study:

To review the chemistry of calcium and its binding properties.
To discuss current research and controversies in mitochondrial calcium signaling.
To explore the role of mitochondrial calcium overload in excitotoxicity and neurodegeneration.

Main Methods:

Literature review of calcium chemistry and mitochondrial function.
Discussion of methodologies for measuring intracellular calcium.
Analysis of calcium overload models in neurotoxicity.

Main Results:

Mitochondrial calcium uptake, sequestration, and release are vital for neuronal function.
Calcium overload in mitochondria contributes to excitotoxic injury and neurodegeneration.
Delayed calcium dysregulation, mitochondrial permeability transition, and reactive oxygen species generation are interconnected.

Conclusions:

Mitochondrial calcium dynamics are central to neuronal signaling and survival.
Understanding mitochondrial calcium handling is key to addressing neurodegenerative conditions.
A unified model of excitotoxicity involving NMDA receptors is proposed, linking calcium overload and mitochondrial dysfunction.