Impairment in eyeblink classical conditioning in adult rats exposed to ethanol as neonates

Background: Eyeblink classical conditioning is a learning task that engages well-defined neural circuitry in the cerebellum and brainstem. Binge-like exposure to alcohol during the neonatal brain growth spurt in rats produces neurotoxic effects on both the cerebellum and the brainstem. The precise l ocalization of the neural substrates of eyeblink conditioning makes it an i deal task to study functional disruptions in the cerebellum and brainstem c aused by early exposure to alcohol. The purpose of this study was to determ ine whether impairments in eyeblink conditioning caused by neonatal binge e xposure to alcohol persist into adulthood, indicative of long-lasting abnor malities in cerebellar and brainstem function. Methods: Group Ethanol received alcohol doses of 5.25 g/kg/day via intragas tric intubation on postnatal days 4-9. Group Sham Intubated underwent the i ntragastric intubation procedures on postnatal days 4-9 but did not receive any infusions. Group Nonintubated did not receive any intubations. When al l rats were at least 3 months old, they were tested in either paired or unp aired eyeblink conditioning. Results: Group Ethanol showed impaired eyeblink conditioning and some abnor malities in conditioned response timing. Control groups did not differ from each Ether. Conclusions: The present data indicate that early exposure to alcohol has l ong-term effects on eyeblink conditioning, perhaps through enduring effects associated with alcohol-induced loss of Purkinje cells of the cerebellum.