RGD Reference Report - Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas. - Rat Genome Database

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Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas.

Authors: El Rawas, Rana  Klement, Sabine  Salti, Ahmad  Fritz, Michael  Dechant, Georg  Saria, Alois  Zernig, Gerald 
Citation: El Rawas R, etal., Front Behav Neurosci. 2012 Mar 2;6:8. doi: 10.3389/fnbeh.2012.00008. eCollection 2012.
RGD ID: 401851084
Pubmed: PMID:22403532   (View Abstract at PubMed)
PMCID: PMC3291868   (View Article at PubMed Central)
DOI: DOI:10.3389/fnbeh.2012.00008   (Journal Full-text)

The worsening of drug abuse by drug-associated social interaction is a well-studied phenomenon. In contrast, the molecular mechanisms of the beneficial effect of social interaction, if offered as a mutually exclusive choice to drugs of abuse, are under-investigated. In a rat place preference conditioning (CPP) paradigm, four 15 min episodes of social interaction with a gender- and weight-matched male early-adult conspecific inhibited cocaine-induced reinstatement of cocaine CPP, a model of relapse. These protective effects of social interaction were paralleled by a reduced activation, as assessed by Zif268 expression, in brain areas known to play pivotal roles in drug-seeking behavior. Here we show that social interaction during extinction of cocaine CPP also reduced cocaine-CPP-stimulated FosB expression in the nucleus accumbens shell and core. In addition, social interaction during cocaine CPP extinction increased pCREB (cAMP response element binding protein) expression in the nucleus accumbens shell and the cingulate cortex area 1 (Cg1). Our results show that FosB and pCREB may be implicated in the protective effect of social interaction against cocaine-induced reinstatement of CPP. Thus, social interaction, if offered in a context that is clearly distinct from the previously drug-associated one, may profoundly inhibit relapse to cocaine addiction.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
FOSBHumancocaine dependence amelioratesISOFosb (Rattus norvegicus) RGD 
FosbRatcocaine dependence amelioratesIEP  RGD 
FosbMousecocaine dependence amelioratesISOFosb (Rattus norvegicus) RGD 

Gene-Chemical Interaction Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
FOSBHumancocaine increases expression ISOFosb (Rattus norvegicus)Cocaine increases expression of Fosb protein in brainRGD 
FosbRatcocaine increases expression EXP Cocaine increases expression of Fosb protein in brainRGD 
FosbMousecocaine increases expression ISOFosb (Rattus norvegicus)Cocaine increases expression of Fosb protein in brainRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
FosbRatresponse to cocaine  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Fosb  (FosB proto-oncogene, AP-1 transcription factor subunit)

Genes (Mus musculus)
Fosb  (FBJ osteosarcoma oncogene B)

Genes (Homo sapiens)
FOSB  (FosB proto-oncogene, AP-1 transcription factor subunit)


Additional Information