Abstract
Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype-a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion regulation, and is altered in the presence of stress, suggesting a mechanism by which REM sleep may impact psychiatric illness. REM sleep shows a developmental progression and increases during adolescence-a period of rapid maturation of the emotional centers of the brain. This study uses a behavioral genetics approach to understand the relative contribution of genes, shared environmental and unique environmental factors to REM sleep neurophysiology in adolescents. Eighteen monozygotic (MZ; n = 36; 18 females) and 12 dizygotic (DZ; n = 24; 12 females) same-sex twin pairs (mean age = 12.46; SD = 1.36) underwent whole-night high-density sleep EEG recordings. We find a significant genetic contribution to REM sleep EEG power across frequency bands, explaining, on average, between 75 to 88% of the variance in power, dependent on the frequency band. In the lower frequency bands between delta and sigma, however, we find an additional impact of shared environmental factors over prescribed regions. We hypothesize that these regions may reflect the contribution of familial and environmental stress shared amongst the twins. The observed strong genetic contribution to REM sleep EEG power in early adolescence establish REM sleep neurophysiology as a potentially strong endophenotype, even in adolescence-a period marked by significant brain maturation.