title: Dopamine transporters in striatum correlate with deactivation in the default mode network during visuospatial attention.
abstract: BACKGROUND
  Dopamine and dopamine transporters (DAT, which regulate extracellular dopamine in the brain) are implicated in the modulation of attention but their specific roles are not well understood. Here we hypothesized that dopamine modulates attention by facilitation of brain deactivation in the default mode network (DMN). Thus, higher striatal DAT levels, which would result in an enhanced clearance of dopamine and hence weaker dopamine signals, would be associated to lower deactivation in the DMN during an attention task.
  
  
  RESULTS
  For this purpose we assessed the relationship between DAT in striatum (measured with positron emission tomography and [(11)C]cocaine used as DAT radiotracer) and brain activation and deactivation during a parametric visual attention task (measured with blood oxygenation level dependent functional magnetic resonance imaging) in healthy controls. We show that DAT availability in caudate and putamen had a negative correlation with deactivation in ventral parietal regions of the DMN (precuneus, BA 7) and a positive correlation with deactivation in a small region in the ventral anterior cingulate gyrus (BA 24/32). With increasing attentional load, DAT in caudate showed a negative correlation with load-related deactivation increases in precuneus.
  
  
  CONCLUSIONS
  These findings provide evidence that dopamine transporters modulate neural activity in the DMN and anterior cingulate gyrus during visuospatial attention. Our findings suggest that dopamine modulates attention in part by regulating neuronal activity in posterior parietal cortex including precuneus (region involved in alertness) and cingulate gyrus (region deactivated in proportion to emotional interference). These findings suggest that the beneficial effects of stimulant medications (increase dopamine by blocking DAT) in inattention reflect in part their ability to facilitate the deactivation of the DMN.
authors: National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. tomasi@bnl.gov
authors: Dardo
authors: D
authors: Tomasi
authors: Nora D
authors: ND
authors: Volkow
authors: Ruiliang
authors: R
authors: Wang
authors: Frank
authors: F
authors: Telang
authors: Gene-Jack
authors: GJ
authors: Wang
authors: Linda
authors: L
authors: Chang
authors: Thomas
authors: T
authors: Ernst
authors: Joanna S
authors: JS
authors: Fowler
mesh_terms: D000328:Adult; D001288:Attention; D001921:Brain / Q000000981:diagnostic imaging* / Q000378:metabolism; D001931:Brain Mapping / Q000379:methods; D002250:Carbon Radioisotopes / Q000494:pharmacology; D003042:Cocaine / Q000494:pharmacology; D003342:Corpus Striatum / Q000378:metabolism*; D050483:Dopamine Plasma Membrane Transport Proteins / Q000378:metabolism*; D006801:Humans; D007091:Image Processing, Computer-Assisted / Q000379:methods; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008954:Models, Biological; D049268:Positron-Emission Tomography / Q000379:methods; D014785:Vision, Ocular
chemical_list: D002250:Carbon Radioisotopes; D050483:Dopamine Plasma Membrane Transport Proteins; D003042:Cocaine