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Slow-wave sleep is reduced and fragmented in adults exposed to high levels of alcohol in the womb, a mouse model shows.
The research, led by Donald A. Wilson, PhD of NYU School of Medicine in New York, and colleagues was published in Neuroscience.
“We have known for a long time that sleep fragmentation is associated with impaired cognitive function, attention and emotional regulation,” Dr Wilson said in statement. “Our study shows for the first time that binge alcohol exposure early in life results in long-lasting slow-wave sleep fragmentation, which, in turn, is associated with learning problems.”
In this study, researchers sought to explore whether slow-wave sleep activity correlated with cognitive and behavioral outcomes in a mouse model of fetal alcohol syndrome.
Mice were injected with binge amounts of ethanol 7 days postnatal, which reflects the third trimester of brain development in a human fetus. Slow-wave analysis was completed using a single electrode implanted in the frontal cortex. Mice exposed to ethanol spent less time in slow-wave sleep and experienced more severe sleep fragmentation, both of which are linked to memory impairment, compared to mice that were injected with saline. Ethanol mice were also hyperactive, and displayed reduced and fragmented slow-wave sleep and increase sleep/wake transitions over 24-hour time intervals compared to control mice. Circadian cycles were not significantly affected.
The ethanol mice also showed impaired contextual fear conditioning memory, which was found to be significantly correlated with slow-wave sleep fragmentation.
“Targeting therapeutic interventions toward sleep may help to relieve aspects of the diverse disorders linked to fetal alcohol exposure, and may open new avenues for treatment of this far too common condition,” Dr Wilson said.
