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Abstract
Sleep loss elevates mitochondrial reactive oxygen species in dFB neurons, which may enhance sleep-promoting activity.
- Two types of potassium channels in fruit fly neurons regulate the balance between waking and sleeping states.
- Oxidative byproducts from mitochondria influence the activity of sleep-inducing neurons through a specific cofactor.
- Increased reactive oxygen species during sleep loss lead to changes in the electrical activity of these neurons.
- The conversion of a key protein to a different form promotes sleep by enhancing action potential frequency.
- Energy metabolism, oxidative stress, and sleep are interconnected processes that may influence aging and disease.
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