Dataset Information

Alcohol gains access to appetitive learning through adolescent heavy drinking.

ABSTRACT: Adolescent heavy alcohol drinking increases the risk for alcohol use disorders in adulthood, yet mechanisms conferring increased risk are not well understood. We propose that adolescent alcohol drinking shapes alcohol's aversive or appetitive properties in adulthood. Alcohol normally drives aversive learning and alcohol-predictive cues are avoided. We hypothesize that through adolescent heavy drinking alcohol gains access to appetitive learning. A primary consequence is that alcohol-predictive cues become valued and sought out. To test this hypothesis, we gave genetically heterogeneous, male Long Evans rats voluntary, chronic intermittent access to water or alcohol throughout adolescence and then identified moderate and heavy alcohol drinkers. After a short abstinence period, we assessed the aversive or appetitive properties of alcohol using flavor learning procedures. We compared alcohol to the known appetitive properties of sugar. Flavor learning in adult rats who were alcohol-naïve or adolescent moderate alcohol drinkers revealed alcohol to be aversive and sugar to be appetitive. The same flavor learning procedures revealed both alcohol and sugar to be appetitive in adult rats who were adolescent heavy drinkers. The results demonstrate that alcohol gains access to neurobehavioral circuits for appetitive learning through adolescent heavy alcohol drinking.

SUBMITTER: DiLeo A

PROVIDER: S-EPMC4874812 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Alcohol gains access to appetitive learning through adolescent heavy drinking.

DiLeo Alyssa A Wright Kristina M KM Mangone Elizabeth E McDannald Michael A MA

Behavioral neuroscience 20150608 4

Adolescent heavy alcohol drinking increases the risk for alcohol use disorders in adulthood, yet mechanisms conferring increased risk are not well understood. We propose that adolescent alcohol drinking shapes alcohol's aversive or appetitive properties in adulthood. Alcohol normally drives aversive learning and alcohol-predictive cues are avoided. We hypothesize that through adolescent heavy drinking alcohol gains access to appetitive learning. A primary consequence is that alcohol-predictive c ...[more]

PMID: 26052793

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Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 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 to 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 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 the in biological processes involved in 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 (WGCNA) 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 long-term changes in neuronal function. Differences in gene expression in the central nucleus of the amygdala (CeA) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.

Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 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 ‚Äì 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 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 the in biological processes involved in 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 (WGCNA) 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 long-term changes in neuronal function. Differences in gene expression in brain nucleus accumbens shell (Acb-sh) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.

Dataset Information

Alcohol gains access to appetitive learning through adolescent heavy drinking.

Publications

Alcohol gains access to appetitive learning through adolescent heavy drinking.

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