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@ARTICLE{Hawkins:893882,
author = {Hawkins, Peter C. T. and Zelaya, Fernando O. and O'Daly,
Owen and Holiga, Stefan and Dukart, Jürgen and Umbricht,
Daniel and Mehta, Mitul A.},
title = {{T}he effect of risperidone on reward‐related brain
activity is robust to drug‐induced vascular changes},
journal = {Human brain mapping},
volume = {42},
number = {9},
issn = {1097-0193},
address = {New York, NY},
publisher = {Wiley-Liss},
reportid = {FZJ-2021-02894},
pages = {2766 - 2777},
year = {2021},
abstract = {Dopamine (DA) mediated brain activity is intimately linked
to reward-driven cerebralresponses, while aberrant reward
processing has been implicated in several
psychiatricdisorders. fMRI has been a valuable tool in
understanding the mechanism by which DAmodulators alter
reward-driven responses and how they may exert their
therapeuticeffect. However, the potential effects of a
pharmacological compound on aspects ofneurovascular coupling
may cloud the interpretability of the BOLD contrast. Here,
weassess the effects of risperidone on reward driven BOLD
signals produced by rewardanticipation and outcome, while
attempting to control for potential drug effects onregional
cerebral blood flow (CBF) and cerebrovascular reactivity
(CVR). Healthy malevolunteers (n = 21) each received a
single oral dose of either 0.5 mg, 2 mg of risperi-done or
placebo in a double-blind, placebo-controlled, randomised,
three-period cross-over study design. Participants underwent
fMRI scanning while performing the widelyused Monetary
Incentive Delay (MID) task to assess drug impact on reward
function.Measures of CBF (Arterial Spin Labelling) and
breath-hold challenge induced BOLD sig-nal changes (as a
proxy for CVR) were also acquired and included as
covariates. Risperi-done produced divergent, dose-dependent
effects on separate phases of rewardprocessing, even after
controlling for potential nonneuronal influences on the
BOLDsignal. These data suggest the D2 antagonist risperidone
has a wide-ranging influenceon DA-mediated reward function
independent of nonneuronal factors. We also illus-trate that
assessment of potential vascular confounds on the BOLD
signal may beadvantageous when investigating CNS drug action
and advocate for the inclusion ofthese additional measures
into future study designs.},
cin = {INM-7},
ddc = {610},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {5253 - Neuroimaging (POF4-525)},
pid = {G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)16},
pubmed = {33666305},
UT = {WOS:000625860700001},
doi = {10.1002/hbm.25400},
url = {https://juser.fz-juelich.de/record/893882},
}