Background: The valuation of risks and the speed with which decisions are made and acted upon are important characteristics of everyone’s personality. These characteristics exist along a continuum that ranges from weak to strong expressions of impulsivity. In certain situations it is crucial to decide and react quickly. Yet these qualities can prove disadvantageous if they are expressed excessively and persistently.
Self-reports, such as the Barratt Impulsiveness Scale, inquire long-term patterns of behavior to assess the level of trait impulsivity. Experimental paradigms, on the other hand, quantify specific impulsive facets, which depend rather on the current environment and state of the individual. These paradigms include decision-making tasks that capture impulsive facets such as the attitudes towards delays, risks and losses.
Research indicates that these attitudes are governed by a valuation network of cortical and subcortical brain regions along with several neurotransmitters. Within this intricate network, frontostriatal circuits innervated by dopamine were identified as an important locus of control. Although a wealth of studies have subsequently examined the influence of the dopaminergic system on impulsive choice, the regulatory mechanisms remain largely unclear. This may originate from the interrelations within the valuation network but also from the complexity of the dopaminergic system itself.
Seminal investigations have shown that this complicated interplay may be partly explained by an underlying inverted U-shaped function, which describes an optimal level of dopamine, flanked by increasing impulsivity in the context of sub- and supraoptimal signaling.
Research Question: This work aimed to shed more light on the inverted-U theory by characterizing the contribution of dopaminergic signaling to trait and decisional impulsivity, and by clarifying whether the manipulation of decisional impulsivity through boosting striatal dopamine via L-DOPA depends on baseline signaling.
We hypothesized that individuals with optimal striatal dopaminergic signaling as measured by [18F]DOPA positron emission tomography would feature low trait impulsivity as assessed with the Barratt Impulsiveness Scale. By contrast, individuals with suboptimal signaling were hypothesized to exhibit stronger trait impulsivity corresponding to higher scores on the Barratt Impulsiveness Scale. Assuming an inverted U-shaped function, we predicted that the dopamine precursor L-DOPA would
reduce impulsive decisions in the latter but overdose individuals with an already optimal signaling and thus make their choice behavior more impulsive.
Materials and Methods: The present studies combined trait and choice measures of impulsivity with the investigation of the dopaminergic system by positron emission tomography and a pharmacological manipulation.
In a double-blind, randomized, placebo-controlled, counter-balanced, repeated measures design, 87 healthy adults completed a computerized decision-making test battery. The battery includes four tasks, each of which captures one distinct dimension of impulsive choice: a delay discounting task quantifies delay discounting, a probability discounting for gains task quantifies risk-seeking for gains, a probability discounting for losses task quantifies risk-seeking for losses and a mixed gambles task quantifies loss aversion. In order to test for baseline-dependent L-DOPA effects on these dimensions, we controlled for trait impulsivity (a suggested proxy for central dopamine) as assessed with the Barratt Impulsiveness Scale (N = 87) and striatal dopamine as measured by [18F]DOPA positron emission tomography (in 60 of the 87 participants).
Results: Our findings highlight the complex role of dopamine in impulsivity and the heterogeneity of its underlying biology.
Participants who scored relatively high on the Barratt Impulsiveness Scale appeared to benefit from L-DOPA, indicated by a decrease in delay discounting, risk-seeking for gains and loss aversion. Participants with low levels of impulsive personality traits as assessed with the Barratt Impulsiveness Scale, on the other hand, exhibited opposite changes in choice preference. Bearing in mind that trait impulsivity may be a behavioral expression of central dopamine, our results suggest an inverted U-shaped function in which impulsive decision-making arises from both sub- and supraoptimal dopaminergic activity.
We found further support for an inverted U-shaped function when accounting for baseline dopamine as measured by [18F]DOPA positron emission tomography. Participants who had higher values on the Barratt Impulsiveness Scale featured low, presumably suboptimal, striatal dopamine signaling. After enhancing and possibly optimizing the basal signaling with L-DOPA, they discounted delays less and tended to less risk-seeking for gains and loss aversion. By contrast, participants with low trait impulsivity as assessed with the Barratt Impulsiveness Scale exhibited higher striatal dopamine,
probably corresponding to optimal baseline activity as L-DOPA shifted their choice behavior in the opposite direction, thus indicating a dopamine overdose.
The intake of L-DOPA had no influence on risk-seeking for losses, even when differences in trait impulsivity and basal levels of striatal dopamine were considered.
Performance on tasks of the decision-making battery produced only few, weak intercorrelations, which implies that delay discounting, risk-seeking for gains, risk-seeking for losses and loss aversion represent dissociable aspects of choice.
Conclusions: Our results endorse and extend previous findings that indicated an inverted U-shaped influence of dopamine on delay discounting and decisions under risk. Utilizing a battery of largely independent choice tasks, we were able to disentangle the effect of gains and losses on risky decisions. Whereas risk-seeking for gains seemed to depend on baseline dopamine signaling, we found no evidence for dopaminergic neurotransmission affecting risk-seeking for losses.
Consistent with the literature, our data shows that self-reported trait impulsivity and experimentally measured decision-making dimensions are distinct phenomena within the multidimensional construct of impulsivity. Our analyses further revealed that choice measures were differentially related to dopaminergic activity, which suggests that they represent not merely descriptive distinctions but separable psychobiological decision-making processes.
Since the regulation of choice probably spreads across neurotransmitter systems, more research on these systems is warranted. After identifying the precise mechanisms within each system, comprehensive studies of their interplay may ultimately uncover how impulsive decisions arise. Considering a series of studies that related steep delay discounting and excessive risk-seeking to poor health and mental illness, the acquired knowledge may also inform translational research on impulsivity-related maladies.