Chronic maternal ethanol consumption results in decreased serotonergic 5-HT1 sites in cerebral cortical regions from offspring.

This laboratory previously demonstrated that chronic maternal ethanol consumption results in a marked deficiency of cortical serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) and of 5-HT uptake sites in the 19- and 35-day-old offspring. In order to determine whether in utero exposure to ethanol similarly affects other components of the serotonergic system we examined the influence of chronic maternal ethanol consumption on cortical, serotonergic 5-HT1 binding sites in developing offspring. Female Sprague-Dawley rats were pair-fed, using control or 6.6% (v/v) ethanol liquid diets on a chronic basis prior to parturition. Serotonergic 5-HT1 sites were measured in synaptosomal membranes from whole cortex and cortical regions from developing offspring. Serotonergic 5-HT1 sites were assessed by measuring the binding of [3H]-5-HT to synaptosomal membranes in the presence and absence of nonradioactive 5-HT. Serotonergic 5-HT2 sites were blocked by including 100 nM spiperone in the assay buffer. The results demonstrated that the 19- and 37-day-old offspring of ethanol-fed rats had a significant (approximately 10-40%) reduction in the Bmax for serotonergic 5-HT1 binding sites on synaptosomal membranes from whole cortex (p less than 0.025), motor cortex (p less than 0.01), and somatosensory cortex (p less than 0.025). However, the binding affinity (Kd) for serotonin was not significantly altered (p greater than 0.05). These results emphasize the sensitivity of the developing cortical serotonergic system to prenatal ethanol exposure.