Linked Life Data

18262797

Source:http://linkedlifedata.com/resource/pubmed/id/18262797

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-3-24
pubmed:abstractText
The telencephalic dopamine innervations contribute to the modulation of cognitive processing. However, the relationship between cognitive effects of D(2/3)-receptor antagonism and dopamine transmission is not described in healthy subjects. We therefore tested effects of acute haloperidol (5 mg/d over 3 days) on continuous performance task (CPT) performance and 6-[(18)F]-fluoro-l-DOPA (FDOPA) PET parameters. Nine physically and mentally healthy male men performed two FDOPA-PET scans including arterial plasma withdrawal. Over 3 days before the second scan, all subjects were treated with 5 mg/d haloperidol orally. Using our novel steady-state analysis, we calculated the intrinsic rate of the cerebral FDOPA utilization (K), the turnover of [(18)F]fluorodopamine formed in brain (k(loss)) and the storage for FDOPA and its brain metabolites (V(d)). Furthermore, a ds-CPT and EPS-screening was performed before every PET scan. We found that FDOPA kinetics in those normal subjects with relatively high baseline K showed a more pronounced sensitivity to haloperidol treatment, manifesting in reduced storage capacity and elevated turnover of [(18)F]fluorodopamine, whereas subjects with lower K showed the opposite pattern of responses. Furthermore, low baseline K predicted improvements in the CPT task after haloperidol, whereas participants with higher baseline K showed a decline in cognitive performance. We conclude that the initial increase of [(18)F]fluorodopamine turnover after acute haloperidol challenge is associated with an over-stimulation in individuals with initially more pharmacologically responsive dopamine systems, but optimizes cognitive performance in those with lower normal FDOPA utilization at baseline. We hypothesize that these effects may be driven by D(1)-receptor mediated transmission during D(2) blockade.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1053-8119
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1222-31
pubmed:meshHeading
pubmed-meshheading:18262797-Adult, pubmed-meshheading:18262797-Algorithms, pubmed-meshheading:18262797-Brain, pubmed-meshheading:18262797-Brain Chemistry, pubmed-meshheading:18262797-Cognition, pubmed-meshheading:18262797-Data Interpretation, Statistical, pubmed-meshheading:18262797-Dopamine, pubmed-meshheading:18262797-Dopamine Antagonists, pubmed-meshheading:18262797-Female, pubmed-meshheading:18262797-Fluorodeoxyglucose F18, pubmed-meshheading:18262797-Haloperidol, pubmed-meshheading:18262797-Humans, pubmed-meshheading:18262797-Image Processing, Computer-Assisted, pubmed-meshheading:18262797-Male, pubmed-meshheading:18262797-Middle Aged, pubmed-meshheading:18262797-Neuropsychological Tests, pubmed-meshheading:18262797-Positron-Emission Tomography, pubmed-meshheading:18262797-Predictive Value of Tests, pubmed-meshheading:18262797-Psychomotor Performance, pubmed-meshheading:18262797-Radiopharmaceuticals, pubmed-meshheading:18262797-Receptors, Dopamine D2, pubmed-meshheading:18262797-Receptors, Dopamine D3
pubmed:year
2008
pubmed:articleTitle
Baseline [18F]-FDOPA kinetics are predictive of haloperidol-induced changes in dopamine turnover and cognitive performance: A positron emission tomography study in healthy subjects.
pubmed:affiliation
Department of Psychiatry and Psychotherapy, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany. ivernaleken@ukaachen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't