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dc.contributor.authorGauthier, Jamie M.
dc.contributor.authorLin, Amy
dc.contributor.authorDhonnchadha, Brid Aine Nic
dc.contributor.authorSpealman, Roger D.
dc.contributor.authorMan, Heng-Ye
dc.contributor.authorKantak, Kathleen M.
dc.date.accessioned2019-02-08T18:17:22Z
dc.date.available2019-02-08T18:17:22Z
dc.date.issued2017-01-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000393902700012&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationJamie M Gauthier, Amy Lin, Brid A Nic Dhonnchadha, Roger D Spealman, Heng-Ye Man, Kathleen M Kantak. 2017. "Environmental enrichment facilitates cocaine-cue extinction, deters reacquisition of cocaine self-administration and alters AMPAR GluA1 expression and phosphorylation." ADDICTION BIOLOGY, Volume 22, Issue 1, pp. 152 - 162 (11). https://doi.org/10.1111/adb.12313
dc.identifier.issn1355-6215
dc.identifier.issn1369-1600
dc.identifier.urihttps://hdl.handle.net/2144/33300
dc.description.abstractThis study investigated the combination of environmental enrichment (EE) with cocaine‐cue extinction training on reacquisition of cocaine self‐administration. Rats were trained under a second‐order schedule for which responses were maintained by cocaine injections and cocaine‐paired stimuli. During three weekly extinction sessions, saline was substituted for cocaine but cocaine‐paired stimuli were presented. Rats received 4‐h periods of EE at strategic time points during extinction training, or received NoEE. Additional control rats received EE or NoEE without extinction training. One week later, reacquisition of cocaine self‐administration was evaluated for 15 sessions, and then GluA1 expression, a cellular substrate for learning and memory, was measured in selected brain regions. EE provided both 24 h before and immediately after extinction training facilitated extinction learning and deterred reacquisition of cocaine self‐administration for up to 13 sessions. Each intervention by itself (EE alone or extinction alone) was ineffective, as was EE scheduled at individual time points (EE 4 h or 24 h before, or EE immediately or 6 h after, each extinction training session). Under these conditions, rats rapidly reacquired baseline rates of cocaine self‐administration. Cocaine self‐administration alone decreased total GluA1 and/or pSer845GluA1 expression in basolateral amygdala and nucleus accumbens. Extinction training, with or without EE, opposed these changes and also increased total GluA1 in ventromedial prefrontal cortex and dorsal hippocampus. EE alone increased pSer845GluA1 and EE combined with extinction training decreased pSer845GluA1 in ventromedial prefrontal cortex. EE might be a useful adjunct to extinction therapy by enabling neuroplasticity that deters relapse to cocaine self‐administration.en_US
dc.description.sponsorshipThe authors declare no competing financial interests. These studies were supported by NSF grant SMA-0835976 to the CELEST Science of Learning Center at Boston University and by NIH grants DA024315 (KMK) and MH079407 (HYM). We thank Iris Mile, Zachary Silber, Sharone Moverman and Enjana Bylykbashi for expert technical assistance. (SMA-0835976 - NSF; DA024315 - NIH; MH079407 - NIH)en_US
dc.description.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798903/en_US
dc.format.extentp. 152-162en_US
dc.languageEnglishen_US
dc.language.isoen_USen_US
dc.publisherWileyen_US
dc.relation.ispartofAddiction biologyen_US
dc.subjectScience & technologyen_US
dc.subjectLife sciences & biomedicineen_US
dc.subjectBiochemistry & molecular biologyen_US
dc.subjectSubstance useen_US
dc.subjectCocaineen_US
dc.subjectCocaine-cue extinction learningen_US
dc.subjectEnvironmental enrichmenten_US
dc.subjectGluA1 receptoren_US
dc.subjectReacquisitionen_US
dc.subjectSelf-administrationen_US
dc.subjectD-cycloserineen_US
dc.subjectSynaptic plasticityen_US
dc.subjectSeeking behavioren_US
dc.subjectReceptor traffickingen_US
dc.subjectBasolateral amygdalaen_US
dc.subjectNeurotrophic factoren_US
dc.subjectNucleus-accumbensen_US
dc.subjectReduces cocaineen_US
dc.subjectUp-regulationen_US
dc.subjectBrainen_US
dc.subjectAnimalsen_US
dc.subjectBehavior, addictiveen_US
dc.subjectConditioning, operanten_US
dc.subjectCuesen_US
dc.subjectDopamine uptake inhibitorsen_US
dc.subjectEnvironmenten_US
dc.subjectExtinction, psychologicalen_US
dc.subjectMaleen_US
dc.subjectPhosphorylationen_US
dc.subjectRatsen_US
dc.subjectReceptors, AMPAen_US
dc.subjectSelf administrationen_US
dc.subjectAlpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic aciden_US
dc.subjectExtinction, psychologicalen_US
dc.subjectEnvironmental enrichmenten_US
dc.subjectMedical and health sciencesen_US
dc.subjectPsychology and cognitive sciencesen_US
dc.subjectSubstance useen_US
dc.titleEnvironmental enrichment facilitates cocaine-cue extinction, deters reacquisition of cocaine self-administration and alters AMPAR GluA1 expression and phosphorylationen_US
dc.typeArticleen_US
dc.description.versionPublished versionen_US
dc.identifier.doi10.1111/adb.12313
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Arts & Sciencesen_US
pubs.organisational-groupBoston University, College of Arts & Sciences, Department of Biologyen_US
pubs.organisational-groupBoston University, College of Arts & Sciences, Department of Psychological & Brain Sciencesen_US
pubs.publication-statusPublisheden_US
dc.identifier.orcid0000-0002-3530-3066 (Man, Heng-Ye)
dc.identifier.orcid0000-0003-1866-9485 (Kantak, Kathleen M)


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