<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Baumgartner HM</submitter><funding>NIDA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Institutes of Health</funding><funding>National Institute on Drug Abuse</funding><pagination>e0267345</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9064096</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(5)</volume><pubmed_abstract>Corticotropin releasing factor (CRF) systems in limbic structures are posited to mediate stress-induced relapse in addiction, traditionally by generating distress states that spur drug consumption as attempts at hedonic self-medication. Yet evidence suggests that activating CRF-expressing neurons in the central amygdala (CeA) or nucleus accumbens (NAc) can magnify incentive motivation in absence of distress, at least for sucrose rewards. However, traditional CRF hypotheses in addiction neuroscience are primarily directed toward drug rewards. The question remains open whether CRF systems can similarly act via incentive motivation mechanisms to promote pursuit of drug rewards, such as cocaine. Here we tested whether optogenetic excitation of CRF-containing neurons in either NAc medial shell,</pubmed_abstract><journal>PloS one</journal><pubmed_title>Corticotropin releasing factor (CRF) systems: Promoting cocaine pursuit without distress via incentive motivation.</pubmed_title><pmcid>PMC9064096</pmcid><funding_grant_id>F31 DA047738</funding_grant_id><funding_grant_id>DA015188</funding_grant_id><funding_grant_id>T32 DA007281</funding_grant_id><funding_grant_id>R01 DA015188</funding_grant_id><funding_grant_id>MH063649</funding_grant_id><funding_grant_id>R01 MH063649</funding_grant_id><pubmed_authors>Schulkin J</pubmed_authors><pubmed_authors>Granillo M</pubmed_authors><pubmed_authors>Berridge KC</pubmed_authors><pubmed_authors>Baumgartner HM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Corticotropin releasing factor (CRF) systems: Promoting cocaine pursuit without distress via incentive motivation.</name><description>Corticotropin releasing factor (CRF) systems in limbic structures are posited to mediate stress-induced relapse in addiction, traditionally by generating distress states that spur drug consumption as attempts at hedonic self-medication. Yet evidence suggests that activating CRF-expressing neurons in the central amygdala (CeA) or nucleus accumbens (NAc) can magnify incentive motivation in absence of distress, at least for sucrose rewards. However, traditional CRF hypotheses in addiction neuroscience are primarily directed toward drug rewards. The question remains open whether CRF systems can similarly act via incentive motivation mechanisms to promote pursuit of drug rewards, such as cocaine. Here we tested whether optogenetic excitation of CRF-containing neurons in either NAc medial shell,</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T13:33:27.48Z</modification><creation>2025-02-19T00:37:48.874Z</creation></dates><accession>S-EPMC9064096</accession><cross_references><pubmed>35503756</pubmed><doi>10.1371/journal.pone.0267345</doi></cross_references></HashMap>