Human Developmental Neurobiology Unit (Gail Tripp)



All organisms learn to adapt to their environment on the basis of the consequences of their actions. When this process goes awry disordered behaviour emerges. One such example is Attention Deficit Hyperactivity Disorder (ADHD). Emerging in childhood, the disorder is diagnosed on the basis of persistent and developmentally-inappropriate levels of overactivity, inattention and impulsivity which interfere with the affected child’s academic, social, and behavioural functioning. The cause of ADHD is not known. There is accumulating evidence that children with ADHD differ from other children in their response to positive reinforcement. This is apparent in their general behaviour and has been demonstrated in a variety of experimental paradigms. Altered sensitivity to reinforcement has important implications both for understanding the brain mechanisms underlying ADHD and for the development of more effective behavioural and pharmacological interventions.

A central goal for our Unit is to clarify the nature and extent of altered sensitivity to positive reinforcement in children whose behaviour is consistent with a diagnosis of ADHD. Specifically we wish to determine (a) which aspects of reinforcement (e.g., frequency, delay, magnitude) differentially affect the behaviour of children with and without ADHD, and (b) whether altered sensitivity to reinforcement is a fundamental characteristic of ADHD, defines a subtype of the disorder, or is a more general characteristic of disordered behaviour. This work will be carried out here in our new Children’s Research Centre at OIST and with our collaborators at the University of Otago, New Zealand.

A second key goal for the unit, in collaboration with the Wickens Neurobiology Unit, is to elucidate the neurobiological basis underlying the altered sensitivity to positive reinforcement seen in children with ADHD. It is well established, through animal studies, that the neurotransmitter dopamine plays a crucial role in the processing of reinforcement and learning. We recently proposed a specific theory of altered dopamine functioning, the Dopamine Transfer Deficit hypothesis (DTD), regarding changes in dopamine signalling that might account for the altered sensitivity to positive reinforcement observed in children with ADHD. This theory makes specific and testable predictions about reinforcement sensitivity in children with ADHD and in animal models of the disorder. These specific predictions will be tested with children meeting criteria for ADHD as part of the Human Developmental Neurobiology Unit’s research activity and with animal models of the disorder in the collaborating Neurobiology Unit.

In the longer term the results of these studies will contribute to a greater understanding of the mechanisms underlying altered sensitivity to reinforcement and possibly ADHD. This knowledge will contribute to the development of more effective behavioural and pharmacological interventions for this chronic and debilitating disorder. The research findings may also offer new directions for identifying which children require assessment for ADHD.

Research Strategies

To achieve these goals we have established the Children’s Research Center at the Okinawa Institute of Science and Technology Graduate University. Children participating in the Research Center’s activities will complete comprehensive assessments to identify their strengths and difficulties before engaging in a range of computerized tasks/activities to determine their sensitivity to different aspects of reinforcement. We also hope to establish Outreach Centers to enable us to include as many families as possible in our research activities.