The present study examined behavioral sensitivity and acute tolerance to ethanol in infants with or without a moderate prenatal ethanol experience. During gestational days 17-20 dams received 0.0 or 2.0 g/kg ethanol. On postnatal day 13 pups were administered 0.0, 0.5 or 2.5 g/kg ethanol prior to assessment of locomotion. One third of the pups were evaluated at 5-10, 30-35 and 60-65 min after ethanol administration; another third was tested only during the last two post-administration periods; and the remaining third was tested only at 60-65 min. At 30-35 min blood ethanol levels were similar to those attained at 60-65 min. The main results of the study were: (a) The 2.5 g/kg ethanol dose induced biphasic motor effects: stimulation 5-10 minutes after drug administration and sedation after 30-35 or 60-65 minutes. (b) Infants exhibited acute tolerance to ethanol's sedative effects. (c) Although pups prenatally treated with ethanol exhibited heightened locomotor activity levels, acute sensitivity and tolerance were not affected by prenatal treatment. In summary, infants are sensitive to biphasic motor consequences of ethanol and readily exhibit acute tolerance to ethanol's sedative effects. In addition, moderate prenatal ethanol exposure was sufficient to induce hyper-reactivity in the offspring without affecting habituation.
KeyboardsPrenatal ethanol; ethanol acute sensitivity; ethanol acute tolerance; locomotor activity; habituation; infant and rat There is a considerable body of experimental evidence indicating that prenatal exposure to ethanol can critically modulate subsequent ethanol intake. This association between prenatal ethanol exposure and later affinity for the drug has been detected in various strains of rats and mice when using a variety of modes of ethanol exposure during pregnancy (Chotro, Arias, & Laviola, 2007). Heightened ethanol consumption resulting from gestational exposure to ethanol has been observed through tests conducted during different ontogenetic periods, including infancy, adolescence and adulthood (Chotro et al., 2007;. Recent epidemiologic studies have found results analogous to those reported in this preclinical research. Even when controlling genetic and environmental factors known to modulate ethanol * Corresponding author. Center for Developmental Psychobiology, Binghamton University, Binghamton, NY 13902-6000, USA Email Address afelicidade@yahoo.es. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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