Maternal ethanol consumption: lack of effect on synaptogenesis in layer I of the motor cortex in 19-day-old rat offspring.

Previous studies showed that in utero exposure to ethanol has an adverse effect on development of the central nervous system. Included among those abnormalities is the evidence that in utero exposure to ethanol alters the development of the cerebral cortex in terms of the arborization of pyramidal dendrites and the concentration of neurotransmitters and neurotransmitter receptors. However, limited information is available about the influence of in utero exposure to ethanol on synaptogenesis in the cortex. We examined the influence of chronic maternal ethanol consumption, prior to parturition, on synaptogenesis in layer I of the motor cortex of 19-day-old-rat offspring. Layer I (the molecular layer) was chosen because of the early timing of its development. The motor cortex was chosen because of the evidence of motor problems in children afflicted with the fetal alcohol syndrome. The results of these studies demonstrated that the 19-day-old offspring of rats that were pair-fed, using control or 6.6% (v/v) ethanol-containing liquid diets on a chronic basis prior to parturition, had a comparable density of synapses and distribution of paramembranous density lengths in layer I of the motor cortex as well as a comparable thickness of cortical layer I. Thus, evidence by this and other laboratories, of cortical neurotransmitter and dendritic abnormalities are not reflected in synaptic changes in layer I of the motor cortex at 19 days. It is possible that synaptogenesis is affected at another age or in other regions of the cerebral cortex.