Giles Story
My research involves building models of human learning and behaviour, with a view to understanding mental illness and ultimately helping people to cope with it.
I completed a PhD in 2015 with the Institute of Global Health Innovation at Imperial College London, in collaboration with the Wellcome Trust Centre for Neuroimaging at UCL, supervised by Professors Ray Dolan, Ara Darzi and Ivo Vlaev.
Address: London, England, United Kingdom
I completed a PhD in 2015 with the Institute of Global Health Innovation at Imperial College London, in collaboration with the Wellcome Trust Centre for Neuroimaging at UCL, supervised by Professors Ray Dolan, Ara Darzi and Ivo Vlaev.
Address: London, England, United Kingdom
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of human morality and is disturbed in antisocial
behavior [1–4]. Deficient harm aversion
may underlie instrumental and reactive aggression,
which both feature in psychopathy [5]. Past
work has highlighted monoaminergic influences
on aggression [6–11], but a mechanistic account
of how monoamines regulate antisocial motives
remains elusive. We previously observed that
most people show a greater aversion to inflicting
pain on others than themselves [12]. Here, we
investigated whether this hyperaltruistic disposition
is susceptible to monoaminergic control. We
observed dissociable effects of the serotonin reuptake
inhibitor citalopram and the dopamine
precursor levodopa on decisions to inflict pain
on oneself and others for financial gain. Computational
models of choice behavior showed that
citalopram increased harm aversion for both self
and others, while levodopa reduced hyperaltruism.
The effects of citalopram were stronger than those
of levodopa. Crucially, neither drug influenced the
physical perception of pain or other components
of choice such as motor impulsivity or loss aversion
[13, 14], suggesting a direct and specific influence
of serotonin and dopamine on the valuation
of harm. We also found evidence for dose
dependency of these effects. Finally, the drugs
had dissociable effects on response times, with
citalopram enhancing behavioral inhibition and
levodopa reducing slowing related to being responsible
for another’s fate. These distinct roles
of serotonin and dopamine in modulating moral
behavior have implications for potential treatments
of social dysfunction that is a common
feature as well as a risk factor for many psychiatric
disorders
of human morality and is disturbed in antisocial
behavior [1–4]. Deficient harm aversion
may underlie instrumental and reactive aggression,
which both feature in psychopathy [5]. Past
work has highlighted monoaminergic influences
on aggression [6–11], but a mechanistic account
of how monoamines regulate antisocial motives
remains elusive. We previously observed that
most people show a greater aversion to inflicting
pain on others than themselves [12]. Here, we
investigated whether this hyperaltruistic disposition
is susceptible to monoaminergic control. We
observed dissociable effects of the serotonin reuptake
inhibitor citalopram and the dopamine
precursor levodopa on decisions to inflict pain
on oneself and others for financial gain. Computational
models of choice behavior showed that
citalopram increased harm aversion for both self
and others, while levodopa reduced hyperaltruism.
The effects of citalopram were stronger than those
of levodopa. Crucially, neither drug influenced the
physical perception of pain or other components
of choice such as motor impulsivity or loss aversion
[13, 14], suggesting a direct and specific influence
of serotonin and dopamine on the valuation
of harm. We also found evidence for dose
dependency of these effects. Finally, the drugs
had dissociable effects on response times, with
citalopram enhancing behavioral inhibition and
levodopa reducing slowing related to being responsible
for another’s fate. These distinct roles
of serotonin and dopamine in modulating moral
behavior have implications for potential treatments
of social dysfunction that is a common
feature as well as a risk factor for many psychiatric
disorders