SNc neurons' Achilles heel

Welberg, Leonie

doi:10.1038/nrn2968

Research Highlight
Published: 08 December 2010

Neurodegenerative disease

SNc neurons' Achilles heel

Leonie Welberg

Nature Reviews Neuroscience volume 12, page 7 (2011)Cite this article

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Dopaminergic SNc neurons show spontaneous, pacemaker-like firing that opens L-type Ca²⁺ channels. This could create an oxidative burden on mitochondria because Ca²⁺ has to be removed by pumps that burn energy that the mitochondria supply through oxidative phosphorylation. Pacemaking also occurs in dopamine neurons in the ventral tegmental area (VTA), but much less Ca²⁺ is allowed to enter here. Because VTA neurons are less affected in Parkinson's disease than SNc neurons, the authors investigated whether Ca²⁺ entry actually creates a measurable mitochondrial oxidative stress.

Monitoring the oxidation of mitochondrial matrix proteins revealed that basal mitochondrial oxidative stress was higher in SNc neurons than in VTA neurons in slices from mature — but not from juvenile — wild-type mice, and higher still in SNc neurons from DJ-1 knockout mice. These differences disappeared when L-type Ca²⁺ channels or Ca²⁺ entry into mitochondria were pharmacologically blocked.

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ORIGINAL RESEARCH PAPER

Guzman, J. N. et al. Oxidant stress evoked by pacemaking in dopaminergic neurons is attenuated by DJ-1. Nature 10 Nov 2010 (doi: 10.1038/nature09536)
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