Journal
CELL CALCIUM
Volume 47, Issue 2, Pages 175-182Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.ceca.2009.12.003
Keywords
Substantia nigra; Dopamine; Mitochondria; Channel; Cav1.3
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Funding
- Hartman Foundation
- USAMRMC
- NIH [NS047085]
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Parkinson's disease (PD) is the second most common neurodegenerative disease in developed countries. The core motor symptoms are attributable to the degeneration of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). Why these neurons, and other restricted sets of non-dopamine neuron, succumb in PD is not clear. One potential clue has come from the observation that the engagement of L-type Ca(2+) channels during autonomous pacemaking elevates the sensitivity of SNc DA neurons to mitochondrial toxins used to create animal models of PD, suggesting that Ca(2+) entry is a factor in their selective vulnerability. Epidemiological data also supports a linkage between L-type Ca(2+) channels and the risk of developing PD. This review examines the hypothesis that the primary factor driving neurodegenerative changes in PD is the metabolic stress created by sustained Ca(2+) entry, particularly in the face of genetic or environmental factors that compromise oxidative defenses or proteostatic competence. (C) 2009 Elsevier Ltd. All rights reserved.
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