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Optogenetic Manipulation of Neural Circuits During Monitoring Sleep/wakefulness States in Mice
Published on: June 19, 2019
The BDNF Val66Met polymorphism modulates sleep intensity: EEG frequency- and state-specificity
Valérie Bachmann1, Carina Klein, Sereina Bodenmann
1Institute of Pharmacology and Toxicology, University of Zürich, Switzerland.
Sleep
|March 2, 2012
Summary
Brain-derived neurotrophic factor (BDNF) gene variations impact sleep intensity. Individuals with the Val/Val genotype exhibit higher sleep slow wave activity, suggesting BDNF influences sleep
Area of Science:
- Neuroscience
- Sleep Science
- Genetics
Background:
- Sleep slow waves are crucial for deep NREM sleep and restorative functions.
- Brain-derived neurotrophic factor (BDNF) is implicated in the homeostatic regulation of sleep slow waves.
- The Val66Met polymorphism in BDNF affects mature BDNF secretion, potentially influencing sleep regulation.
Purpose of the Study:
- To investigate if the BDNF Val66Met polymorphism contributes to individual differences in human sleep slow wave activity (SWA).
Main Methods:
- Study conducted in a temporal isolation unit with participants undergoing 40 hours of prolonged wakefulness.
- Compared 11 Val/Val homozygotes with 11 heterozygous Met allele carriers (Val/Met).
- Assessed cognitive performance, subjective state, and electroencephalogram (EEG) during waking and sleep.
Main Results:
- Val/Val homozygotes demonstrated superior working memory performance compared to Val/Met carriers.
- EEG sleep slow wave activity (SWA) was significantly higher in Val/Val individuals during baseline and recovery sleep.
- These differences in SWA were most prominent during the initial NREM sleep episodes.
Conclusions:
- Genetic variations in BDNF influence the regulation of sleep slow wave oscillations.
- Neuronal plasticity, modulated by genetic factors like the BDNF polymorphism, plays a role in determining NREM sleep intensity.
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