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Updated: Jun 28, 2026
The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
Published on: August 5, 2017
Neonatal binge alcohol exposure produces dose dependent deficits in interstimulus interval discrimination eyeblink
Kevin L Brown1, Michael A Burman, Huan B Duong
1University of Delaware, USA. brownkev@temple.edu
Insights
Neonatal alcohol exposure impairs eyeblink classical conditioning (EBC) in juvenile rats. This study shows dose-dependent deficits in interstimulus interval (ISI) discrimination, suggesting greater sensitivity to alcohol
Area of Science:
- Neuroscience
- Developmental Psychology
- Toxicology
Background:
- Neonatal alcohol exposure models human fetal alcohol spectrum disorders.
- Alcohol-induced cerebellar damage impacts motor learning.
- Eyeblink classical conditioning (EBC) assesses cerebellar function.
Purpose of the Study:
- To investigate the effects of neonatal alcohol exposure on EBC in juvenile rats.
- To assess interstimulus interval (ISI) discrimination in alcohol-exposed juveniles.
- To compare alcohol's effects on EBC in juveniles versus adults.
Main Methods:
- Neonatal rats received daily alcohol doses (3-5 g/kg/day) or controls from postnatal days 4-9.
- Juveniles (postnatal day 30) underwent ISI discrimination training.
- Conditioned response (CR) acquisition and CR latency were measured.
Main Results:
- Alcohol-exposed juveniles showed dose-dependent deficits in ISI discrimination.
- CR latency was not significantly affected by neonatal alcohol exposure.
- Alcohol-induced EBC impairments may be more pronounced in adult rats compared to juveniles.
Conclusions:
- Neonatal alcohol exposure impairs complex motor learning (ISI discrimination EBC) in juvenile rats.
- ISI discrimination EBC is sensitive to moderate levels of neonatal alcohol exposure.
- Developmental stage influences the severity of alcohol-induced EBC deficits.
Abstract:
Alcohol consumption in neonatal rats produces cerebellar damage and is widely used to model 3rd-trimester human fetal alcohol exposure. Neonatal "binge-like" exposure to high doses of alcohol (5 g/kg/day or more) impairs acquisition of eyeblink classical conditioning (EBC), a cerebellar-dependent Pavlovian motor learning task. We have recently found impairments in interstimulus interval (ISI) discrimination--a complex task variant of EBC--in adult rats following postnatal day (PD) 4-9 alcohol exposure at doses of 3, 4, and 5 g/kg/day. Because robust developmental differences in conditioned response (CR) generation and CR latency measures are present between untreated juveniles and adults in this task, we sought to extend alcohol findings to juvenile rats (PD30). Five neonatal treatment groups were used: (1) undisturbed controls, (2) sham intubation controls, (3) 3 g/kg/day of alcohol (blood alcohol concentration {BAC}=139.9 mg/dl), (4) 4 g/kg/day of alcohol (BAC=237.3 mg/dl), or (5) 5 g/kg/day of alcohol (BAC=301.8 mg/dl). Intubations occurred over PD4-9. ISI discrimination training in juveniles (PD30-33) revealed dose-dependent CR deficits in all three alcohol-exposed groups relative to controls. Contrary to expected outcomes, CR latency measures were not significantly affected as a function of neonatal treatment. Comparison of these findings with our recent study in adults suggests that alcohol-induced impairments in ISI discrimination EBC may be greater in adults relative to juveniles. The present findings provide further evidence that ISI discrimination may provide greater sensitivity to functional deficits resulting from moderate levels of neonatal alcohol exposure relative to single-cue EBC paradigms.
