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Impairment in Eyeblink Classical Conditioning in Adult Rats Exposed to Ethanol as Neonates
Author(s) -
Green John T.,
Rogers Ronald F.,
Goodlett Charles R.,
Steinmetz Joseph E.
Publication year - 2000
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2000.tb02010.x
Subject(s) - eyeblink conditioning , cerebellum , brainstem , classical conditioning , conditioning , psychology , medicine , anesthesia , neuroscience , statistics , mathematics
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 localization of the neural substrates of eyeblink conditioning makes it an ideal task to study functional disruptions in the cerebellum and brainstem caused by early exposure to alcohol. The purpose of this study was to determine whether impairments in eyeblink conditioning caused by neonatal binge exposure to alcohol persist into adulthood, indicative of long‐lasting abnormalities in cerebellar and brainstem function. Methods: Group Ethanol received alcohol doses of 5.25 g/kg/day via intragastric intubation on postnatal days 4–9. Group Sham Intubated underwent the intragastric intubation procedures on postnatal days 4–9 but did not receive any infusions. Group Nonintubated did not receive any intubations. When all rats were at least 3 months old, they were tested in either paired or unpaired eyeblink conditioning. Results: Group Ethanol showed impaired eyeblink conditioning and some abnormalities in conditioned response timing. Control groups did not differ from each other. Conclusions: The present data indicate that early exposure to alcohol has long‐term effects on eyeblink conditioning, perhaps through enduring effects associated with alcohol‐induced loss of Purkinje cells of the cerebellum.