Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8351443 | Pharmacology Biochemistry and Behavior | 2014 | 9 Pages |
Abstract
The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by male adolescent alcohol-preferring (P) rats. Starting at 28Â days of age, P rats were given concurrent access to 15 and 30% ethanol for 3 one-h sessions/day for 5 consecutive days/week for 3Â weeks. Rats were killed by decapitation 3Â h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5-3.0Â g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDRÂ =Â 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in biological processes involved with cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce changes in neuronal function.
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Authors
William J. McBride, Mark W. Kimpel, Jeanette N. McClintick, Zheng-Ming Ding, Howard J. Edenberg, Tiebing Liang, Zachary A. Rodd, Richard L. Bell,