Abstract

There is substantial evidence to suggest that ethanol exposure during vulnerable periods of prenatal somatic growth results in a number of morphological abnormalities and cognitive deficits in offspring. Amongst the characteristics exhibited by affected individuals are abnormal sleeping patterns, particularly abnormal rapid eye movement (REM) sleep. To better understand how prenatal ethanol exposure specifically affects sleeping patterns in offspring, an animal model of fetal alcohol syndrome was investigated using the Sprague–Dawley rat. Our study demonstrated that the amount of time spent in REM sleep was reduced in female, but not male rats, which were exposed to ethanol in utero as compared to male and female saline controls. Similarly, % REM sleep for female saline control rats was almost twice that of females exposed to ethanol (11.9 vs. 6.9%). By contrast, ethanol treated and control saline males did not differ on the % REM measure (11.5 vs. 10.4%), nor did they differ from the female saline controls. No differences were observed between males and females or treatment groups in terms of time spent in either slow wave sleep or wakefulness.

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