Binge-like alcohol exposure of neonatal rats via intragastric intubation induces both Purkinje cell loss and cortical astrogliosis.

Binge-like alcohol exposure in neonatal rats on postnatal days 4 to 9 via artificial rearing results in a well-documented transient astrogliosis in the cerebral cortex. A recent study, which replicated the astrogliosis using artificial rearing, found that alcohol administered via daily exposure cycles in a vapor inhalation chamber on postnatal days 4 to 9 failed to elicit the effect, thus suggesting that the gliosis was an interactive effect of the artificial rearing administration and not specific to alcohol. The present study evaluated the effects in an intragastric intubation model that replicated the dosing parameters of the artificial rearing while avoiding the stress of surgery and extended maternal separation. In coronal frozen sections through parietal cortex labeled immunohistochemically for glial fibrillary acidic protein, the pups exposed to alcohol by intubation had a significantly greater density of glial fibrillary acidic protein-positive astrocytes per unit volume, compared with littermate controls intubated with a maltose-dextrin formula; alcohol also induced fibrillary hypertrophy of the labeled astrocytes. In the cerebellum, alcohol induced a significant reduction in Purkinje cell number as determined using the optical disector method. These outcomes extend previous findings that neonatal binge alcohol exposure induces acute cortical astrogliosis and Purkinje cell loss, and confirm that the alcohol-induced astrogliosis is not an artifact of artificial rearing.