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Article: Mesocorticolimbic circuits are impaired in chronic cocaine users as demonstrated by resting-state functional connectivity

TitleMesocorticolimbic circuits are impaired in chronic cocaine users as demonstrated by resting-state functional connectivity
Authors
Issue Date2010
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynimg
Citation
Neuroimage, 2010, v. 53 n. 2, p. 593-601 How to Cite?
AbstractPreclinical models have consistently demonstrated the importance of the mesocorticolimbic (MCL) brain reward system in drug dependence, with critical molecular and cellular neuroadaptations identified within these structures following chronic cocaine administration. Cocaine dependent individuals manifest alterations in reward functioning that may relate to changes induced by cocaine or to pre-existing differences related to vulnerability to addiction. The circuit level manifestations of these drug-induced plastic changes and predispositions to drug dependence are poorly understood in preclinical models and virtually unknown in human drug dependence. Using whole-brain resting-state fMRI connectivity analysis with 'seed voxels' placed within individual nodes of the MCL system, we report network-specific functional connectivity strength decreases in cocaine users within distinct circuits of the system, including between ventral tegmental area (VTA) and a region encompassing thalamus/lentiform nucleus/nucleus accumbens, between amygdala and medial prefrontal cortex (mPFC), and between hippocampus and dorsal mPFC. Further, regression analysis on regions showing significant functional connectivity decrease in chronic cocaine users revealed that the circuit strength between VTA and thalamus/lentiform nucleus/nucleus accumbens was negatively correlated with years of cocaine use. This is the first evidence of circuit-related changes in human cocaine dependence and is consistent with the range of cognitive and behavioral disruptions seen in cocaine dependence. As potential circuit level biomarkers of cocaine dependence, these circuit alterations may be usefully applied in treatment development and monitoring treatment outcome. © 2010.
Persistent Identifierhttp://hdl.handle.net/10722/169876
ISSN
2023 Impact Factor: 4.7
2023 SCImago Journal Rankings: 2.436
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGu, Hen_HK
dc.contributor.authorSalmeron, BJen_HK
dc.contributor.authorRoss, TJen_HK
dc.contributor.authorGeng, Xen_HK
dc.contributor.authorZhan, Wen_HK
dc.contributor.authorStein, EAen_HK
dc.contributor.authorYang, Yen_HK
dc.date.accessioned2012-10-25T04:57:30Z-
dc.date.available2012-10-25T04:57:30Z-
dc.date.issued2010en_HK
dc.identifier.citationNeuroimage, 2010, v. 53 n. 2, p. 593-601en_HK
dc.identifier.issn1053-8119en_HK
dc.identifier.urihttp://hdl.handle.net/10722/169876-
dc.description.abstractPreclinical models have consistently demonstrated the importance of the mesocorticolimbic (MCL) brain reward system in drug dependence, with critical molecular and cellular neuroadaptations identified within these structures following chronic cocaine administration. Cocaine dependent individuals manifest alterations in reward functioning that may relate to changes induced by cocaine or to pre-existing differences related to vulnerability to addiction. The circuit level manifestations of these drug-induced plastic changes and predispositions to drug dependence are poorly understood in preclinical models and virtually unknown in human drug dependence. Using whole-brain resting-state fMRI connectivity analysis with 'seed voxels' placed within individual nodes of the MCL system, we report network-specific functional connectivity strength decreases in cocaine users within distinct circuits of the system, including between ventral tegmental area (VTA) and a region encompassing thalamus/lentiform nucleus/nucleus accumbens, between amygdala and medial prefrontal cortex (mPFC), and between hippocampus and dorsal mPFC. Further, regression analysis on regions showing significant functional connectivity decrease in chronic cocaine users revealed that the circuit strength between VTA and thalamus/lentiform nucleus/nucleus accumbens was negatively correlated with years of cocaine use. This is the first evidence of circuit-related changes in human cocaine dependence and is consistent with the range of cognitive and behavioral disruptions seen in cocaine dependence. As potential circuit level biomarkers of cocaine dependence, these circuit alterations may be usefully applied in treatment development and monitoring treatment outcome. © 2010.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynimgen_HK
dc.relation.ispartofNeuroImageen_HK
dc.subject.meshAdulten_US
dc.subject.meshBrain Mappingen_US
dc.subject.meshCerebral Cortex - Pathologyen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshCocaine-Related Disorders - Pathology - Psychologyen_US
dc.subject.meshCuesen_US
dc.subject.meshData Interpretation, Statisticalen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLimbic System - Pathologyen_US
dc.subject.meshMagnetic Resonance Imagingen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNeural Pathways - Pathologyen_US
dc.subject.meshResten_US
dc.subject.meshSocioeconomic Factorsen_US
dc.subject.meshSubstance-Related Disorders - Pathologyen_US
dc.titleMesocorticolimbic circuits are impaired in chronic cocaine users as demonstrated by resting-state functional connectivityen_HK
dc.typeArticleen_HK
dc.identifier.emailGeng, X: gengx@hku.hken_HK
dc.identifier.authorityGeng, X=rp01678en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neuroimage.2010.06.066en_HK
dc.identifier.pmid20603217-
dc.identifier.scopuseid_2-s2.0-77956061301en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956061301&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume53en_HK
dc.identifier.issue2en_HK
dc.identifier.spage593en_HK
dc.identifier.epage601en_HK
dc.identifier.isiWOS:000281688000023-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridGu, H=35233258000en_HK
dc.identifier.scopusauthoridSalmeron, BJ=6603367393en_HK
dc.identifier.scopusauthoridRoss, TJ=7203043487en_HK
dc.identifier.scopusauthoridGeng, X=34771310000en_HK
dc.identifier.scopusauthoridZhan, W=7102238668en_HK
dc.identifier.scopusauthoridStein, EA=7202194954en_HK
dc.identifier.scopusauthoridYang, Y=7409387192en_HK
dc.identifier.issnl1053-8119-

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