Mom's high alcohol levels disrupt neonatal brain

Slow-wave sleep — or deep sleep which converts daily events into permanent memories — is fragmented in those adults exposed to high levels of alcohol while in their mother's womb.

According to a study conducted at New York University (NYU), Langone Medical Center and its Nathan S. Kline Institute for Psychiatric Research (NKI), 1 in 100 adults suffer from fetal alcohol disorders linked to a pregnant woman's binge drinking. Alcohol affects the ability of the fetus to learn and build memories. The child and later adult can also have mood problems. Research results are published in the journal Neuroscience.

According to the science, exposure of a developing brain to binge levels of alcohol results in permanent fragmentation of slow-wave sleep.

Slow-wave sleep is non-rapid eye movement sleep. Called slow-wave sleep because EEG activity (electrophysical measurement of voltage from neurons in the brain) is recorded as slow waves with a frequency of less than 1 Hz. Primary physical signs are moderate muscle tone and slow or absent eye movement in sleep. Slow-waves, though, are important in consolidating new memories; adults with insomnia do not do well on memory tasks. Human sleep deprivation studies suggest the primary function of slow-wave sleep is the brain's ability to recover from daily activities. But, sleep deprivation also affects secretion of growth hormone.

"We have known for a long time that sleep fragmentation is associated with impaired intellectual function, attention and regulation of emotion. For the first time, we show that early binge alcohol exposure results in long-lasting slow-wave sleep fragmentation associated with learning problems."

"It appears fetal alcohol syndrome changes the brain's ability to regulate sleep."

Donald Wilson PhD, Professor, Langone Department of Child and Adolescent Psychiatry and Neuroscience and Physiology, New York Universityand, member Nathan S. Kline Institute for Psychiatric Research.

Using a mouse model, researchers injected late pregnancy mice with ethanol alcohol (drinking alcohol) equivalent to consumed alcohol to body volume in human "binge drinking." A control group of pregnant mice were injected with equivalent amounts of non-toxic, benign, saline solution during the same period of pregnancy. Researchers then examined slow-wave sleep in mice pups born to each group of mothers seven days after birth. Mouse pup brains seven days post birth equate with third trimester brain development in a human fetus.

Pups exposed to ethanol spent less time in slow-wave sleep and experienced severe sleep fragmentation, both results consistent with significant memory impairment. Researchers also noted that ethanol-exposed pups were hyperactive, unlike pups of the saline injected control group. Ethanol-dosed pups had reduced and fragmented slow-wave sleep and increased sleep/wake transitions. In addition, they displayed impaired memory of events occurring in context, a result not found in control group pups. The severity of their memory impairment directly correlated to the extent of their sleep fragmentation.

"Targeting therapeutic interventions around sleep may help relieve aspects of disorders linked to fetal alcohol exposure, and may open new avenues for treatment of this far too common condition."

Donald Wilson PhD

Abstract
Developmental ethanol (EtOH) exposure can lead to long-lasting cognitive impairment, hyperactivity, and emotional dysregulation among other problems. In healthy adults, sleep plays an important role in each of these behavioral manifestations. Here we explored circadian rhythms (activity, temperature) and slow-wave sleep (SWS) in adult mice that had received a single day of EtOH exposure on postnatal day 7 and saline littermate controls. We tested for correlations between slow-wave activity and both contextual fear conditioning and hyperactivity. Developmental EtOH resulted in adult hyperactivity within the home cage compared to controls but did not significantly modify circadian cycles in activity or temperature. It also resulted in reduced and fragmented SWS, including reduced slow-wave bout duration and increased slow-wave/fast-wave transitions over 24-h periods. In the same animals, developmental EtOH exposure also resulted in impaired contextual fear conditioning memory. The impairment in memory was significantly correlated with SWS fragmentation. Furthermore, EtOH-treated animals did not display a post-training modification in SWS which occurred in controls. In contrast to the memory impairment, sleep fragmentation was not correlated with the developmental EtOH-induced hyperactivity. Together these results suggest that disruption of SWS and its plasticity are a secondary contributor to a subset of developmental EtOH exposure's long-lasting consequences.

Other study NYU coauthors include Kurt Masiello, Monica Lewin, Maria Hui, John Smiley, and Mariko Saito. The research was supported by a grant to Wilson and Saito from the National Institute on Alcohol Abuse and Alcoholism (R01-AA023181) part of the National Institutes of Health.

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Mar 2, 2016   Fetal Timeline   Maternal Timeline   News   News Archive   

Donald Wilson PhD: "It appears fetal alcohol syndrome changes the brain's ability to regulate sleep."
Image Credit: public domain