@phdthesis{Plichta2009,
  author    = {Plichta, Michael M.},
  title     = {Neural correlates of delay discounting: Effects of dopamine bioavailability and implications for attention-deficit/hyperactivity disorder (ADHD)},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-35953},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {Humans and other animals share choice preference for smaller-but-sooner over later-but-larger rewards, indicating that the subjective value of a reward is discounted as a function of time. This phenomenon referred to as delay discounting (DD), represents one facet of impulsivity which is inherently connected with reward processing and, within a certain range, adaptive. Maladaptive levels, however, can lead to suboptimal decision-making and represent important characteristics of psychopathologies such as attention-deficit/hyperactivity disorder (ADHD). In line with a proposed influence of dysregulated dopamine (DA) levels on impulsivity, neural structures involved in DD (the ventral-striatum [VS]; orbitofrontal cortex [OFC]) are highly innervated by dopaminergic neurons. However, studies explicitly testing the triadic interplay of dopaminergic neurotransmission, impulsivity and brain activation during intertemporal choice are missing. Therefore, the first study of the thesis examined the effect of different DA-bioavailability levels, indicated by a genetic polymorphism (Val158Met) in the gene of the catechol-O-methyltransferase, on the association of delay discounting and OFC activation. OFC response to monetary rewards that varied by delay-to-delivery was recorded with functional near-infrared spectroscopy (fNIRS) in a sample of 49 healthy human subjects. The results suggest a DA-related enhancement in OFC function from low (low DA level) to partial (intermediate DA level) and full (high DA level) reward delay sensitivity. Furthermore, DA-bioavailability was shown to moderate the association of neural reward delay sensitivity and impulsivity: OFC reward delay sensitivity was strongly correlated with impulsivity at intermediate DA-levels, but not at low or high DA-levels where impulsivity was related to delay-independent OFC amplitudes. It is concluded that DA-level should be considered as a crucial factor whenever impulsivity-related brain activation, in particular to reward delay, is examined in healthy subjects. Dysfunctional reward processing, accompanied by a limited ability to tolerate reward delays (delay aversion), has been proposed as an important feature in ADHD putatively caused by striatal hypo-dopaminergia. Therefore, the aim of the second study of this thesis was to examine subcortical processing of reward delays and to test for neural indicators of a negative emotional response to delay periods. Using functional magnetic resonance imaging (fMRI), brain activation in adult patients with ADHD (n=14) and healthy control subjects (n=12) was recorded during the processing of immediate and delayed rewards. Compared with healthy control subjects, hyporesponsiveness of the VS reward system was evident in patients with ADHD for both immediate and delayed rewards. In contrast, delayed rewards evoked hyperactivation in the dorsal caudate nucleus and the amygdala of ADHD patients, corroborating the central predictions of the delay aversion hypothesis. In combination both studies support the conception of a close link between delay discounting, brain activation and dopaminergic neurotransmission. The results implicate that studies on neural correlates of DD have to account for the DA-bioavailability level and for a negative emotional response to reward delays.},
  subject      = {Impulsivit{\"a}t},
  language  = {en}
}