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.