Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0005946
DC FieldValue
dc.titleCocaine modulates locomotion behavior in C. elegans
dc.contributor.authorWard A.
dc.contributor.authorWalker V.J.
dc.contributor.authorFeng Z.
dc.contributor.authorXu X.Z.S.
dc.date.accessioned2019-11-08T00:52:49Z
dc.date.available2019-11-08T00:52:49Z
dc.date.issued2009
dc.identifier.citationWard A., Walker V.J., Feng Z., Xu X.Z.S. (2009). Cocaine modulates locomotion behavior in C. elegans. PLoS ONE 4 (6) : e5946. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0005946
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161837
dc.description.abstractCocaine, a potent addictive substance, is an inhibitor of monoamine transporters, including DAT (dopamine transporter), SERT (serotonin transporter) and NET (norepinephrine transporter). Cocaine administration induces complex behavioral alterations in mammals, but the underlying mechanisms are not well understood. Here, we tested the effect of cocaine on C. elegans behavior. We show for the first time that acute cocaine treatment evokes changes in C. elegans locomotor activity. Interestingly, the neurotransmitter serotonin, rather than dopamine, is required for cocaine response in C. elegans. The C. elegans SERT MOD-5 is essential for the effect of cocaine, consistent with the role of cocaine in targeting monoamine transporters. We further show that the behavioral response to cocaine is primarily mediated by the ionotropic serotonin receptor MOD-1. Thus, cocaine modulates locomotion behavior in C. elegans primarily by impinging on its serotoninergic system. � 2009 Ward et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subject4 aminobutyric acid
dc.subjectacetylcholine
dc.subjectcocaine
dc.subjectvesicular monoamine transporter
dc.subjectcocaine
dc.subjectdopamine uptake inhibitor
dc.subjectserotonin
dc.subjectanimal experiment
dc.subjectarticle
dc.subjectCaenorhabditis elegans
dc.subjectconcentration response
dc.subjectgene targeting
dc.subjecthyperactivity
dc.subjectlocomotion
dc.subjectmonoamine release
dc.subjectneuromodulation
dc.subjectnonhuman
dc.subjectserotoninergic system
dc.subjectserotoninergic transmission
dc.subjectstimulus response
dc.subjectallele
dc.subjectanimal
dc.subjectanimal behavior
dc.subjectautomation
dc.subjectbiological model
dc.subjectcocaine dependence
dc.subjectcomputer program
dc.subjectdisease model
dc.subjectdrug effect
dc.subjectgenetics
dc.subjectmovement (physiology)
dc.subjectmutation
dc.subjectpathophysiology
dc.subjectCaenorhabditis elegans
dc.subjectMammalia
dc.subjectAlleles
dc.subjectAnimals
dc.subjectAutomation
dc.subjectBehavior, Animal
dc.subjectCaenorhabditis elegans
dc.subjectCocaine
dc.subjectCocaine-Related Disorders
dc.subjectDisease Models, Animal
dc.subjectDopamine Uptake Inhibitors
dc.subjectModels, Biological
dc.subjectMovement
dc.subjectMutation
dc.subjectSerotonin
dc.subjectSoftware
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pone.0005946
dc.description.sourcetitlePLoS ONE
dc.description.volume4
dc.description.issue6
dc.description.pagee5946
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