<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lloret Torres ME</submitter><funding>National Institute on Alcohol Abuse and Alcoholism</funding><funding>U.S. Department of Defense</funding><funding>Imaging Core at the Institute of Neurobiology National Science Foundation</funding><funding>National Institute on Minority Health and Health Disparities</funding><funding>NIGMS NIH HHS</funding><pagination>e0322576</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12193044</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(6)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Stressor-related disorders frequently co-occur with alcohol use disorder (AUD). This necessitates an understanding of the physiological and genetic factors contributing to this relationship. Binge drinking is the most common method of alcohol consumption among adolescent males and significantly increases the risk of developing comorbid stressor-related disorders and AUD. In experiments modeling the effects of a single binge-like alcohol exposure in male adolescent mice, we observed a clear deficit in context extinction learning. This exposure led to a significant initial increase in subsequent voluntary drinking on day one, as measured by the every-other-day (EOD) two-bottle choice drinking assay, which normalized thereafter.&lt;h4>Methods&lt;/h4>For this study we performed </pubmed_abstract><journal>PloS one</journal><pubmed_title>Comparative mRNA profile analysis from NAc of adolescent male mice after binge-like alcohol exposure eliciting deficits in context fear extinction learning.</pubmed_title><pmcid>PMC12193044</pmcid><funding_grant_id>U54 MD007600</funding_grant_id><funding_grant_id>G12MD 007600</funding_grant_id><funding_grant_id>P20 GM103642</funding_grant_id><funding_grant_id>52680-LS-IS</funding_grant_id><funding_grant_id>P30 GM149367</funding_grant_id><funding_grant_id>1R01AA027808</funding_grant_id><funding_grant_id>DBI-0115825</funding_grant_id><pubmed_authors>Lay Rivera XX</pubmed_authors><pubmed_authors>Ruiz Bolivar DF</pubmed_authors><pubmed_authors>Roche-Lima A</pubmed_authors><pubmed_authors>Pena Seneriz YL</pubmed_authors><pubmed_authors>Florian Alsina JA</pubmed_authors><pubmed_authors>Dieppa Rodriguez M</pubmed_authors><pubmed_authors>Cardona Jordan K</pubmed_authors><pubmed_authors>Lloret Torres ME</pubmed_authors><pubmed_authors>Tosado Rodriguez EL</pubmed_authors><pubmed_authors>Colon Rivera PA</pubmed_authors><pubmed_authors>Garcia Colon JO</pubmed_authors><pubmed_authors>Gonzalez Del Toro J</pubmed_authors><pubmed_authors>Velazquez-Marrero C</pubmed_authors><pubmed_authors>Capella Muniz JL</pubmed_authors><pubmed_authors>Rivas Jimenez A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Comparative mRNA profile analysis from NAc of adolescent male mice after binge-like alcohol exposure eliciting deficits in context fear extinction learning.</name><description>&lt;h4>Introduction&lt;/h4>Stressor-related disorders frequently co-occur with alcohol use disorder (AUD). This necessitates an understanding of the physiological and genetic factors contributing to this relationship. Binge drinking is the most common method of alcohol consumption among adolescent males and significantly increases the risk of developing comorbid stressor-related disorders and AUD. In experiments modeling the effects of a single binge-like alcohol exposure in male adolescent mice, we observed a clear deficit in context extinction learning. This exposure led to a significant initial increase in subsequent voluntary drinking on day one, as measured by the every-other-day (EOD) two-bottle choice drinking assay, which normalized thereafter.&lt;h4>Methods&lt;/h4>For this study we performed </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-04-25T03:30:18.636Z</modification><creation>2026-04-25T03:22:46.882Z</creation></dates><accession>S-EPMC12193044</accession><cross_references><pubmed>40560842</pubmed><doi>10.1371/journal.pone.0322576</doi></cross_references></HashMap>