Chronic prenatal ethanol exposure alters the proportion of GABAergic neurons in layers II/III of the adult guinea pig somatosensory cortex.

Chronic prenatal ethanol exposure increases the expression of gamma-aminobutyric acid type A (GABA(A)) receptors in the adult guinea pig cerebral cortex. One possible explanation for this change in receptor number is the loss of GABAergic innervation and subsequent up-regulation of GABA(A) receptors. We tested this hypothesis by determining the relative proportion of glutamic acid decarboxylase (GAD) immunopositive cells in the cerebral cortex of adult guinea pig offspring that had received chronic daily exposure to ethanol (4 g/kg maternal body weight) throughout gestation. Chronic prenatal exposure to ethanol decreased the number of neurons that were GAD-immunopositive relative to the total number of cresyl-violet-stained neurons by approximately 30% in layers II/III of the adult guinea pig somatosensory cortex. No changes were observed in other cortical layers. These data suggest that chronic prenatal exposure to ethanol results in either a selective loss of GABAergic interneurons or failure to express GAD in layers II/III of the adult guinea pig somatosensory cortex.