<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Bahi, Amine</dc:creator>
  <dc:creator>Dreyer, Jean-Luc</dc:creator>
  <dc:date>2019-11-30</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">During the last few decades, alcohol use disorders (AUD) have reached an epidemic  prevalence, yet social influences on alcoholism have not been fully addressed.  Several factors can modulate alcohol intake. On one hand, stress can reinforce  ethanol-induced behaviors and be an important component in AUD and alcoholism.  On the other hand, environmental enrichment (EE) has a neuroprotective role and  prevents the development of excessive ethanol intake in rodents. However, studies  showing the role of EE in chronic psychosocial stress-impaired ethanol-conditioned  rewards are nonexistent.Aim: The purpose of the current study is to explore the  potential protective role of EE on extinction and reinstatement of ethanol-conditioned  place preference (EtOH-CPP) following chronic psychosocial stress.Methods: In the  first experiment and after the EtOH-CPP test, the mice were subjected to 15 days of  chronic stress, then housed in a standard (SE) or enriched environment (EE) while  EtOH-CPP extinction was achieved by repeated exposure to the CPP chambers  without ethanol injection. In the second experiment and after the EtOH-CPP test,  extinction was achieved as described above. Mice were then exposed to chronic  stress for 2 weeks before being housed in a SE or EE. EtOH-CPP reinstatement was  induced by a single exposure to the conditioning chambers.Results: As expected,  stress exposure increased anxiety-like behavior and reduced weight gain. More  importantly, we found that EE significantly shortened chronic stress-delayed extinction  and decreased the reinstatement of EtOH-CPP.Conclusion: These results support the  hypothesis that EE reduces the impact of alcohol-associated environmental stimuli,  and hence it may be a general intervention for reducing cue-elicited craving and  relapse in humans.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/308321</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/308321/files/dre_eed.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/s00213-019-05408-8</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Psychopharmacology. - 2020, vol. 237, no. 3, p. 707-721</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Environmental enrichment decreases chronic psychosocial stress-impaired extinction and reinstatement of ethanol conditioned place preference in C57BL/6 male mice</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
