Abstract
The most distinguishing feature of neurons is their capacity for regenerative electrical activity. This activity imposes a significant mitochondrial burden, especially in neurons that are autonomously active, have broad action potentials, and exhibit prominent Ca2+ entry. Many of the genetic mutations and toxins associated with Parkinson's disease compromise mitochondrial function, providing a mechanistic explanation for the pattern of neuronal pathology in this disease. Because much of the neuronal mitochondrial burden can be traced to L-type voltagedependent channels (channels for which there are brain-penetrantantagonists approved for human use), a neuroprotective strategy to reduce this burden is available.
Original language | English (US) |
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Pages (from-to) | 10736-10741 |
Number of pages | 6 |
Journal | Journal of Biological Chemistry |
Volume | 288 |
Issue number | 15 |
DOIs | |
State | Published - Apr 12 2013 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology