PMID- 21153806
OWN - NLM
STAT- MEDLINE
DCOM- 20110815
LR  - 20220330
IS  - 1432-2072 (Electronic)
IS  - 0033-3158 (Print)
IS  - 0033-3158 (Linking)
VI  - 215
IP  - 1
DP  - 2011 May
TI  - Modafinil modulation of the default mode network.
PG  - 23-31
LID - 10.1007/s00213-010-2111-5 [doi]
AB  - RATIONALE: The default mode network (DMN) is a functional network which is 
      implicated in a range of cognitive processes. This network is proposed to consist 
      of hubs located in the ventromedial prefrontal cortex (vmPFC), posterior 
      cingulate/retrosplenial cortex (PCC/rSpl), and inferior parietal lobule (IPL), 
      with other midline cortical and temporal lobe nodes connected to these hubs. How 
      this network is modulated by neurochemical systems during functional brain 
      activity is not yet understood. OBJECTIVES: In the present study, we used the 
      norepinephrine/dopamine transporter inhibitor modafinil to test the hypothesis 
      that this drug modulates the DMN. METHODS: Eighteen healthy right-handed adults 
      participated in a double-blind, placebo-controlled study of single oral dose 
      modafinil 200 mg. They performed a simple visual sensorimotor task during slow 
      event-related fMRI. Drug effects were interrogated within the DMN defined by 
      task-induced deactivation (TID) on placebo. RESULTS: There was a trend toward 
      faster reaction time (RT) on modafinil (Cohen's d = 0.38). Brain regions within 
      the DMN which exhibited significant modafinil-induced augmentation of TID 
      included vmPFC, PCC/rSpl, and left IPL. Across subjects, the modafinil effect on 
      TID in the vmPFC was significantly and specifically associated with drug effects 
      on RT speeding. CONCLUSIONS: Modafinil augments TID in the DMN to facilitate 
      sensorimotor processing speed, an effect which may be particularly dependent on 
      changes in vmPFC activity. This is consistent with the gain control function of 
      catecholamine systems and may represent an important aspect of the pro-cognitive 
      effects of modafinil.
FAU - Minzenberg, Michael J
AU  - Minzenberg MJ
AD  - Department of Psychiatry, University of California, Davis School of Medicine, 
      Sacramento, CA, USA. michael.minzenberg@ucdmc.ucdavis.edu
FAU - Yoon, Jong H
AU  - Yoon JH
FAU - Carter, Cameron S
AU  - Carter CS
LA  - eng
GR  - R01 MH059883/MH/NIMH NIH HHS/United States
GR  - UL1 RR024146/RR/NCRR NIH HHS/United States
GR  - MH059883/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, N.I.H., Extramural
DEP - 20101214
PL  - Germany
TA  - Psychopharmacology (Berl)
JT  - Psychopharmacology
JID - 7608025
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (Catecholamines)
RN  - R3UK8X3U3D (Modafinil)
SB  - IM
MH  - Adult
MH  - Benzhydryl Compounds/*pharmacology
MH  - Brain/*drug effects/metabolism/physiology
MH  - Catecholamines/metabolism
MH  - Cognition/*drug effects/physiology
MH  - Cross-Over Studies
MH  - Double-Blind Method
MH  - Female
MH  - Functional Laterality/physiology
MH  - Gyrus Cinguli/drug effects/metabolism/physiology
MH  - Humans
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Modafinil
MH  - Nerve Net/*drug effects/physiology
MH  - Neuropsychological Tests
MH  - Parietal Lobe/drug effects/metabolism/physiology
MH  - Prefrontal Cortex/drug effects/metabolism/physiology
MH  - Psychomotor Performance/*drug effects/physiology
MH  - Reaction Time/drug effects/physiology
MH  - Rest/physiology
PMC - PMC3072511
EDAT- 2010/12/15 06:00
MHDA- 2011/08/16 06:00
PMCR- 2010/12/14
CRDT- 2010/12/15 06:00
PHST- 2010/07/22 00:00 [received]
PHST- 2010/11/22 00:00 [accepted]
PHST- 2010/12/15 06:00 [entrez]
PHST- 2010/12/15 06:00 [pubmed]
PHST- 2011/08/16 06:00 [medline]
PHST- 2010/12/14 00:00 [pmc-release]
AID - 2111 [pii]
AID - 10.1007/s00213-010-2111-5 [doi]
PST - ppublish
SO  - Psychopharmacology (Berl). 2011 May;215(1):23-31. doi: 10.1007/s00213-010-2111-5. 
      Epub 2010 Dec 14.