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On the scent of mitochondrial calcium

Nature Neuroscience volume 15, pages 653–654 (2012)Cite this article

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Odorants are now shown to elevate mitochondrial Ca2+ in sensory neurons; moreover, blocking this Ca2+ sequestration impairs dynamic range. Acute stimulation rapidly recruits mitochondria from the soma to the dendritic knob.

Odor perception begins with the binding of odor molecules to specific G protein–coupled receptors located in the cilia of canonical olfactory sensory neurons (OSNs). This process causes a rise in cyclic AMP that leads to the opening of cAMP-gated, Ca2+-permeable cation channels that, in turn, produce a transient elevation of intracellular Ca2+. Thus, Ca2+ signaling is intimately related to odor sensing, and a detailed understanding of the mechanisms underlying Ca2+ regulation in OSNs is required for a complete understanding of olfactory function. A study by Fluegge et al.1 in this issue of Nature Neuroscience opens a new chapter in this story and shows that mitochondrial Ca2+ regulation contributes to this feat.

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Figure 1: Schematic representation of Ca2+ signaling mechanisms in cilia and dendritic knob of an OSN.

Katie Vicari

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Authors and Affiliations

  1. Frank Zufall is in the Department of Physiology, University of Saarland School of Medicine, Homburg, Germany.,

    Frank Zufall

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  1. Frank Zufall
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Correspondence to Frank Zufall.

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Zufall, F. On the scent of mitochondrial calcium. Nat Neurosci 15, 653–654 (2012). https://doi.org/10.1038/nn.3090

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