Focus on the positive: computational simulations implicate asymmetrical reward prediction error signals in childhood attention-deficit/hyperactivity disorder.
A number of hypotheses have suggested that the principal neurological dysfunction responsible for the behavioural symptoms associated with Attention-Deficit/Hyperactive Disorder (ADHD) is likely rooted in abnormal phasic signals coded by the firing rate of midbrain dopamine neurons. We present a formal investigation of the impact atypical phasic dopamine signals have on behaviour by applying a TD(λ) reinforcement learning model to simulations of operant conditioning tasks that have been argued to quantify the hyperactive, inattentive and impulsive behaviour associated with ADHD. The results presented here suggest that asymmetrically effective dopamine signals encoded by a punctate increase or decrease in dopamine levels provide the best account for the behaviour of children with ADHD as well as an animal model of ADHD, the spontaneously hypertensive rat (SHR). The biological sources of this asymmetry are considered, as are other computational models of ADHD.
Cockburn
Jeffrey
J
Department of Cognitive, Linguistic and Psychological Sciences, Brown University, USA. jeffrey_cockburn@brown.edu
Holroyd
Clay B
CB
D000818:Animals; D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology*; D002648:Child; D003198:Computer Simulation; D004195:Disease Models, Animal; D004298:Dopamine / Q000502:physiology; D006801:Humans; D008960:Models, Psychological; D009434:Neural Pathways / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012201:Reward
D004298:Dopamine