Research Article
Binge-like ethanol exposure during the early postnatal period impairs eyeblink conditioning at short and long CS–US intervals in rats
Tuan D. Tran,
Mark E. Stanton,
Charles R. Goodlett,
Corresponding Author
Tuan D. Tran
Department of Psychology, East Carolina University, Greenville, NC 27858
Department of Psychology, East Carolina University, Greenville, NC 27858Search for more papers by this authorMark E. Stanton
Department of Psychology, University of Delaware, 131 Wolf Hall, Newark, DE 19716
Search for more papers by this authorCharles R. Goodlett
Department of Psychology, Indiana University-Purdue, University at Indianapolis, Indianapolis, IN 46202
Search for more papers by this authorTuan D. Tran,
Mark E. Stanton,
Charles R. Goodlett,
Corresponding Author
Tuan D. Tran
Department of Psychology, East Carolina University, Greenville, NC 27858
Department of Psychology, East Carolina University, Greenville, NC 27858Search for more papers by this authorMark E. Stanton
Department of Psychology, University of Delaware, 131 Wolf Hall, Newark, DE 19716
Search for more papers by this authorCharles R. Goodlett
Department of Psychology, Indiana University-Purdue, University at Indianapolis, Indianapolis, IN 46202
Search for more papers by this authorAbstract
Binge-like ethanol exposure on postnatal days (PD) 4–9 in rodents causes cerebellar cell loss and impaired acquisition of conditioned responses (CRs) during “short-delay” eyeblink classical conditioning (ECC), using optimal (280–350 ms) interstimulus intervals (ISIs). We extended those earlier findings by comparing acquisition of delay ECC under two different ISIs. From PD 4 to 9, rats were intubated with either 5.25 g/kg of ethanol (2/day), sham intubated, or were not intubated. They were then trained either as periadolescents (about PD 35) or as adults (>PD 90) with either the optimal short-delay (280-ms) ISI, a long-delay (880-ms) ISI, or explicitly unpaired CS and US presentations. Neonatal binge ethanol treatment significantly impaired acquisition of conditioning at both ages regardless of ISI, and deficits in the acquisition and expression of CRs were comparable across ISIs. These deficits are consistent with the previously documented ethanol-induced damage to the cerebellar–brainstem circuit essential for Pavlovian ECC. © 2007 Wiley Periodicals, Inc. Dev Psychobiol 49: 589-605, 2007.
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