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dc.contributor.authorJauhar, S
dc.contributor.authorVeronese, M
dc.contributor.authorRogdaki, M
dc.contributor.authorBloomfield, M
dc.contributor.authorNatesan, S
dc.contributor.authorTurkheimer, F
dc.contributor.authorKapur, S
dc.contributor.authorHowes, OD
dc.date.accessioned2021-02-04T00:09:35Z
dc.date.available2021-02-04T00:09:35Z
dc.date.issued2017-02-07
dc.identifierpii: tp2016270
dc.identifier.citationJauhar, S., Veronese, M., Rogdaki, M., Bloomfield, M., Natesan, S., Turkheimer, F., Kapur, S. & Howes, O. D. (2017). Regulation of dopaminergic function: an [F-18]-DOPA PET apomorphine challenge study in humans. TRANSLATIONAL PSYCHIATRY, 7 (2), https://doi.org/10.1038/tp.2016.270.
dc.identifier.issn2158-3188
dc.identifier.urihttp://hdl.handle.net/11343/259043
dc.description.abstractDopaminergic function has a key role in normal brain function, dopaminergic dysfunction being implicated in numerous neuropsychiatric disorders. Animal studies show that dopaminergic stimulation regulates dopaminergic function, but it is not known whether this exists in humans. In the first study (study 1), we measured dopamine synthesis capacity (indexed as Kicer) to identify the relationship between baseline and change in Kicer under resting conditions for comparison with effects of dopaminergic stimulation. In the second study (study 2), we used a within-subjects design to test effects of dopaminergic stimulation on dopamine synthesis capacity. In study 1, eight volunteers received two 18F-DOPA scans on separate days, both at rest. In study 2, 12 healthy male volunteers received two 18F-DOPA positron emission tomographic (PET) scans after treatment with either the dopamine partial agonist apomorphine (0.03 or 0.005 mg kg-1) or placebo. In study 1, no significant correlation was found between baseline and change in dopamine synthesis capacity between scans (r=-0.57, n=8, P=0.17, two-tailed). In study 2, a significant negative correlation was found between baseline dopamine synthesis capacity and percentage change in dopamine synthesis capacity after apomorphine challenge (r=-0.71, n=12, P=0.01, two-tailed). This correlation was significantly different (P<0.01) from the correlation between baseline and change in dopamine synthesis capacity under unstimulated conditions. One-way repeated-measures analysis of variance showed a significant group (study 1/study 2) × time interaction (F(1,18)=11.5, P=0.003). Our findings suggest that regulation of dopamine synthesis capacity by apomorphine depends on baseline dopamine function, consistent with dopamine stimulation stabilizing dopaminergic function. Loss of this autoregulation may contribute to dopaminergic dysfunction in brain disorders such as schizophrenia, substance dependence, and Parkinson's disease.
dc.languageEnglish
dc.publisherNATURE PUBLISHING GROUP
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleRegulation of dopaminergic function: an [F-18]-DOPA PET apomorphine challenge study in humans
dc.typeJournal Article
dc.identifier.doi10.1038/tp.2016.270
melbourne.affiliation.departmentMedicine Dentistry & Health Sciences
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titleTranslational Psychiatry
melbourne.source.volume7
melbourne.source.issue2
dc.rights.licenseCC BY
melbourne.elementsid1197457
melbourne.contributor.authorKapur, Shitij
dc.identifier.eissn2158-3188
melbourne.accessrightsOpen Access


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