The BDNF Val66Met polymorphism modulates sleep intensity: EEG frequency- and state-specificity
| Autor: | Wolfgang Berger, Nikolaus F. Schäfer, Carina Klein, Valérie Bachmann, Hans-Peter Landolt, Peter Brugger, Sereina Bodenmann |
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| Rok vydání: | 2012 |
| Předmět: |
Adult
Male medicine.medical_specialty Time Factors Genotype Electroencephalography Non-rapid eye movement sleep 03 medical and health sciences Young Adult 0302 clinical medicine Memory Physiology (medical) Internal medicine medicine Humans Effects of sleep deprivation on cognitive performance 030304 developmental biology Slow-wave sleep 0303 health sciences Sleep Stages Polymorphism Genetic medicine.diagnostic_test Brain-Derived Neurotrophic Factor Sleep in non-human animals Sleep deprivation Endocrinology Case-Control Studies Commentary Sleep Deprivation Wakefulness Female Neurology (clinical) medicine.symptom Psychology Arousal Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Sleep |
| DOI: | 10.5665/sleep.1690 |
| Popis: | Study objectives EEG slow waves are the hallmark of deep NREM sleep and may reflect the restorative functions of sleep. Evidence suggests that increased sleep slow waves after sleep deprivation reflect plastic synaptic processes, and that brain-derived neurotrophic factor (BDNF) is causally involved in their homeostatic regulation. The functional Val66Met polymorphism of the gene encoding pro-BDNF causes impaired activity-dependent secretion of mature BDNF protein. We investigated whether this polymorphism contributes to the pronounced inter-individual variation in sleep slow wave activity (SWA) in humans. Setting Sleep laboratory in temporal isolation unit. Participants Eleven heterozygous Met allele carriers and 11 individually sex- and age-matched Val/Val homozygotes. Interventions Forty hours prolonged wakefulness. Measurements and results Cognitive performance, subjective state, and waking and sleep EEG in baseline and after sleep deprivation were studied. Val/Val homozygotes showed better response accuracy than Met allele carriers on a verbal 2-back working memory task. This difference did not reflect genotype-dependent differences in sleepiness, well-being, or sustained attention. In baseline and recovery nights, deep stage 4 sleep and NREM sleep intensity as quantified by EEG SWA (0.75-4.5 Hz) were higher in Val/Val compared to Val/Met genotype. Similar to sleep deprivation, the difference was most pronounced in the first NREM sleep episode. By contrast, increased activity in higher EEG frequencies (> 6 Hz) in wakefulness and REM sleep was distinct from the effects of prolonged wakefulness. Conclusion BDNF contributes to the regulation of sleep slow wave oscillations, suggesting that genetically determined variation in neuronal plasticity modulates NREM sleep intensity in humans. |
| Databáze: | OpenAIRE |
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