Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Alcohol and Alcoholism, 2015, 50(S1) i1–i67 Abstracts ESBRA 2015 EUROPEAN SOCIETY FOR BIOMEDICAL RESEARCH ON ALCOHOLISM 12–15 SEPTEMBER 2015 VALENCIA, SPAIN P-03 ETHANOL AFFECTS LIMBIC AND STRIATAL EXPRESSION OF VESICULAR GLUTAMATE TRANSPORTERS IN OUTBRED RATS EXPOSED TO EARLY LIFE STRESS M. Vrettou1, L. Granholm2, A. Todkar1, K. W. Nilsson3, Å. Wallén-Mackenzie1, I. Nylander2, and E. Comasco1 1 Department of Neuroscience, Uppsala University, Uppsala, Sweden, 2 Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden, and 3Västerås Centre for Clinical Research, Uppsala University, Västerås, Sweden Early-life experience can induce adaptive changes in key neurotransmitter systems and contribute to proneness or resilience to alcohol misuse later in life. Glutamate is an important regulator of reward circuits and implicated in alcohol-related phenotypes. In the present study, gene expression of the best known cellular markers for glutamatergic phenotype, Vesicular Glutamate Transporters (Vglut) 1, 2 and 3, was analyzed in outbred rats to investigate cortico-limbic and -striatal genetic signatures in relation to early-life stress (ELS), and consequent propensity to ethanol consumption. Brain regions of interest were the ventral tegmental area (VTA), nucleus accumbens (Acb), medial prefrontal cortex and dorsal striatum (dStr), which subserve the glutamatergic system, are target of environmental influences and involved in several aspects of addiction. Maternal separation conditions were employed to mimic high and less stressful environment during early life, and a two-bottle free-choice paradigm was used to assess ethanol intake in adulthood, modelling human weekend binge-like drinking patterns. Region-specific Vglut expression patterns were observed upon exposure to ethanol in an interaction with ELS in the VTA, Acb, and dStr, while only ethanol-induced effects were noted in the dStr. Correlations between Vgluts expression reflected these effects as they were disturbed when the interactive effect of ELS and ethanol was present, but otherwise Vgluts were highly correlated. These findings suggest that in non-dependent, non-preferring rats, voluntary ethanol consumption, influenced by early-life history, affects glutamatergic presynaptic mechanisms in the VTA and the striatal parts of the brain, which presumably contribute to the transition towards ethanol misuse. © The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved