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@ARTICLE{Kruppa:856981,
author = {Kruppa, Jana and Gossen, Anna and Weiß, Eileen Oberwelland
and Kohls, Gregor and Großheinrich, Nicola and Cholemkery,
Hannah and Freitag, Christine M. and Karges, Wolfram and
Wölfle, Elke and Sinzig, Judith and Fink, Gereon Rudolf and
Herpertz-Dahlmann, Beate and Konrad, Kerstin and
Schulte-Rüther, Martin},
title = {{N}eural modulation of social reinforcement learning by
intranasal oxytocin in male adults with high-functioning
autism spectrum disorder: a randomized trial},
journal = {Neuropsychopharmacology},
volume = {44},
number = {4},
issn = {0893-133X},
address = {Basingstoke},
publisher = {Nature Publishing Group84063},
reportid = {FZJ-2018-06270},
pages = {749-756},
year = {2019},
abstract = {Reduced social motivation is a hallmark of individuals with
autism spectrum disorders (ASDs). Although the exact neural
mechanisms are unclear, oxytocin has been shown to enhance
motivation and attention to social stimuli, suggesting a
potential to augment social reinforcement learning as the
central mechanism of behavioral interventions in ASD. We
tested how reinforcement learning in social contexts and
associated reward prediction error (RPE) signals in the
nucleus accumbens (NAcc) were modulated by intranasal
oxytocin. Male adults with a childhood diagnosis of ASD
(n = 15) and healthy controls (n = 24; aged 18–26
years) performed a probabilistic reinforcement learning task
during functional magnetic resonance imaging in a
single-center (research center in Germany), randomized
double-blind, placebo-controlled cross-over trial. The
interventions were intranasal oxytocin (Syntocinon®,
Novartis; 10 puffs = 20 international units (IUs) per
treatment) and placebo spray. Using computational modeling
of behavioral data, trial-by-trial RPE signals were assessed
and related to brain activation in NAcc during reinforcing
feedback in social and non-social contexts. The order of
oxytocin/placebo was randomized for 60 participants.
Twenty-one participants were excluded from analyses, leaving
39 for the final analysis. Behaviorally, individuals with
ASD showed enhanced learning under oxytocin when the
learning target as well as feedback was social as compared
to non-social (social vs. non-social target: $87.09\%$ vs.
$71.29\%,$ $95\%$ confidence interval (CI): 7.28–24.33,
p = .003; social vs. non-social feedback: $81.00\%$ vs.
$71.29\%,$ $95\%$ CI: 2.81–16.61, p = .027).
Correspondingly, oxytocin enhanced the correlation of the
RPE signal with NAcc activation during social (vs.
non-social) feedback in ASD (3.48 vs. −1.12, respectively,
$95\%$ CI: 2.98–6.22, p = .000), whereas in controls,
this effect was found in the placebo condition (2.90 vs.
−1.14, respectively, $95\%$ CI: 1.07–7.01,
p = .010). In ASD, a similar pattern emerged when the
learning target was social (3.00 vs. −0.64, respectively,
$95\%$ CI: −0.13 to 7.41, p = .057), whereas controls
showed a reduced correlation for social learning targets
under oxytocin (−0.70 vs. 2.72, respectively, $95\%$ CI:
−5.86 to 0.98, p = .008). The current data suggest
that intranasal oxytocin has the potential to enhance social
reinforcement learning in ASD. Future studies are warranted
that investigate whether oxytocin can potentiate social
learning when combined with behavioral therapies, resulting
in greater treatment benefits than traditional behavior-only
approaches.},
cin = {INM-3},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30390065},
UT = {WOS:000458386200012},
doi = {10.1038/s41386-018-0258-7},
url = {https://juser.fz-juelich.de/record/856981},
}