An Explanation for Hyperactivity Following Prenatal Alcohol Exposure

Public awareness of the damaging effects of drinking during pregnancy has resulted in fewer women drinking during pregnancy. However, the percentage of women that drink heavily has not changed. High levels of alcohol during pregnancy can cause lifelong conditions such as Fetal Alcohol Syndrome or Fetal Alcohol Spectrum Disorders. The severity of these effects varies between individuals and many factors have been proposed to explain this variation. We hypothesized that additional challenges to the fetus would increase the severity of prenatal alcohol exposure. For example, brief periods of mild hypoxia (reduced oxygen flow) are common during normal labor and delivery however this may put the alcohol-exposed offspring at increased risk. We used a rodent model to examine whether prenatal alcohol exposure and hypoxia would affect activity levels. Hyperactivity and ADHD occur in nearly 90% of children with an FASD. Male and female rat pups were divided into three treatment groups; an alcohol exposed group (4.5 g/kg/day), an intubated control, and a non-treated control. The alcohol dose was relatively low and given by a feeding tube on postnatal days (PND) 1-7. This exposure period overlaps a period of brain growth that occurs during the human 3rd trimester. On PND 8, the pups were divided into hypoxia or control groups and a brief hypoxic challenge was administered (8.5 min). Activity levels were examined in juvenile rats (PND 20 21) using a circular chamber with activity measured for 30 min daily. Offspring exposed to both the alcohol and hypoxia showed clear hyperactivity in the test chamber. These results show that brief hypoxia worsens the effects of prenatal alcohol exposure. By becoming increasingly aware of the factors that may increase the severity of FASD, we can work to reduce the adverse effects. Supported in part by NIAAA 017956 to SB