Reduced sleep and impaired sleep initiation in adult male rats exposed to alcohol during early postnatal period.

Abstract Prenatal alcohol exposure (AE) is associated with cognitive and neurobehavioral abnormalities, such as increased motor activity and elevated anxiety, that may last a lifetime. Persistent sleep disruption may underlie these problems. Using a rat model, we investigated long-term alterations of sleep–wake behavior following AE during a critical early developmental period. Male rats received 2.6 g/kg of alcohol intragastrically twice daily on postnatal days (PD) 4–9, a developmental period equivalent to the third trimester of human pregnancy (AE group), or were sham-intubated (S group). On PD52–80, they were instrumented for tethered electroencephalogram and nuchal electromyogram recording and habituated to the recording procedures. Sleep–wake behavior was then recorded during one 24 h-long session. Wake, slow-wave sleep (SWS) and rapid eye movement sleep (REMS) were scored in 10 s epochs during 6 h of the lights-on (rest) and 6 h of the lights-off (active) periods. During the active period, REMS percentage was significantly lower (4.7 ± 0.9 (SE) vs. 8.2 ± 0.9; p p  = 0.07) in AE than S rats ( N  = 6/group). During the rest period, sleep and wake amounts did not differ between the groups, but AE rats had longer latency to both SWS and REMS onset ( p  = 0.02 and 0.003, respectively). Our data demonstrate that, in a rat model of prenatal AE, impaired sleep–wake behavior persists into the adulthood. Disordered sleep may exacerbate cognitive and behavioral disorders seen in human victims of prenatal AE.