Research Article Early Maternal Deprivation Enhances Voluntary Alcohol Intake Induced by Exposure to Stressful Events Later in Life Sara Peñasco, 1 Virginia Mela, 1 Jose Antonio López-Moreno, 2 María-Paz Viveros, 1 and Eva M. Marco 1 1 Departamento de Fisiolog´ ıa (Fisiolog´ ıa Animal II), Facultad de Ciencias Biol´ ogicas, Universidad Complutense de Madrid, Instituto de Investigaci´ on Sanitaria del Hospital Cl´ ınico San Carlos (IdISSC), 28040 Madrid, Spain 2 Departamento de Psicobiolog´ ıa, Facultad de Psicolog´ ıa, Universidad Complutense, 28223 Madrid, Spain Correspondence should be addressed to Mar´ ıa-Paz Viveros; pazviver@bio.ucm.es and Eva M. Marco; emmarco@bio.ucm.es Received 15 November 2014; Revised 14 January 2015; Accepted 29 January 2015 Academic Editor: Nina N. Karpova Copyright © 2015 Sara Pe˜ nasco et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In the present study, we aimed to assess the impact of early life stress, in the form of early maternal deprivation (MD, 24h on postnatal day, pnd, 9), on voluntary alcohol intake in adolescent male and female Wistar rats. During adolescence, from pnd 28 to pnd 50, voluntary ethanol intake (20%, v/v) was investigated using the two-bottle free choice paradigm. To better understand the relationship between stress and alcohol consumption, voluntary alcohol intake was also evaluated following additional stressful events later in life, that is, a week of alcohol cessation and a week of alcohol cessation combined with exposure to restraint stress. Female animals consumed more alcohol than males only afer a second episode of alcohol cessation combined with restraint stress. MD did not afect baseline voluntary alcohol intake but increased voluntary alcohol intake afer stress exposure, indicating that MD may render animals more vulnerable to the efects of stress on alcohol intake. During adolescence, when animals had free access to alcohol, MD animals showed lower body weight gain but a higher growth rate than control animals. Moreover, the higher growth rate was accompanied by a decrease in food intake, suggesting an altered metabolic regulation in MD animals that may interact with alcohol intake. 1. Introduction Epidemiological data indicate that adverse life events dur- ing the frst few years of life can increase the risk for psychopathology, including drug addiction [1, 2]. In fact, early life stress has been proposed to predict alcohol drink- ing in adolescence and alcohol abuse and dependence at adulthood (see [3] for review). Alcohol dependence afects millions of people worldwide, and alcohol consumption at adolescence has reached alarming rates [4]. In rodents, the efects of early life stress can be studied in a controlled manner by removal of the dam during the frst 2 weeks of life (for a review on the animals models of dam-litter interaction disruption, please consult [5–7]). Te efects of early life stress on alcohol consumption currently available are inconsistent and highly dependent on environmental factors such as the species and strains used and the protocol used for the maternal separation protocol (see [8] as an example). In rats, repeated maternal separation during early postnatal life (180–360 min. a day during the frst three weeks of life) has been reported to induce an increase in alcohol intake [9–12], although no changes in alcohol consumption have also been reported [13–15]. It is worth mentioning that the investigation of possible sex diferences in this regard has been neglected. In the last years, we have focused on the investigation of the early maternal deprivation (MD) animal model, that is, 24 h of dam-litter separation on postnatal day (pnd) 9. Adolescent animals exposed to MD have been reported to exhibit a trend to increased impulsivity, depressive-like responses, and impairments in cognitive function [16–18]. At adolescence, an increase in striatal dopamine levels has also been reported as a conse- quence of MD, possibly refecting an altered brain reward system [19]. Actually, MD seems to modify the response of Hindawi Publishing Corporation Neural Plasticity Volume 2015, Article ID 342761, 10 pages http://dx.doi.org/10.1155/2015/342761