Bernard Balleine


Image of Bernard Balleine Bernard Balleine received his BA with first class honours and with the university medal from the University of Sydney in 1987, together with the Thomson Prize and Australian Psychological Association Prize for Psychology honours. In 1989 he won a Commonwealth Scholarship and a College Scholarship from Churchill College, Cambridge UK to support research towards his Ph.D in comparative psychology, which he received from the University of Cambridge in 1993. Subsequently, he was elected to a Research Fellowship at Jesus College Cambridge and spent three years conducting post-doctoral research in behavioral neuroscience in the Department of Experimental Psychology at Cambridge University. He was appointed Assistant Professor at the University of California, Los Angeles in 1995 and in 1996 won a FIRST Award from the National Institute of Mental Health. In 2000 he was appointed Associate Professor and in 2004 Full Professor at UCLA which is his current position. He was elected a Fellow of the American Psychological Association in 2004 and in 2005 he was appointed Associate Director for Research in the Brain Research Institute.

Work Address: Office
Franz Hall, 8425A
Los Angeles, CA 90095
UNITED STATES
Work Address: Laboratory
Franz Hall B258
Los Angeles, CA 90095
UNITED STATES

Research Interests

Generally stated, I am interested in the establishing whether and on what basis the classical division of reflex, habit and volition can be maintained, how the sources of these activities differ and how they interact in the neural systems involved in motor, cognitive and emotional functions to determine complex adaptive behavior. As a consequence, my research focuses on the psychological and neural determinants of (1) goal-directed actions (2) their transition into habits and (3) the similarities and differences of these latter with respect to simple conditioned and unconditioned reflexes. I am approaching this issue systematically using mice, rats and, recently, people as subjects and we are using a variety of methods including sophisticated psychological paradigms for investigating cognitive functions such as planning, decision-making and self-control (impulsivity) as well as basic molecular, genetic, pharmacological, electrophysiological, histological and other imaging techniques to investigate the neural processes involved. In our most recent work, these methods have been employed to investigate the role of circuits involving prefrontal cortex and the basal ganglia in goal-directed and habit based learning systems and the way these distinct circuits interact. Disorders of 'voluntary' movement, e.g. in Parkinson's disease, and involving intrusive involuntary movement, e.g. in Tourette's syndrome, obsessive compulsive disorder and Huntingdon's disease, have been found to involve damage to cortico-striatal networks and to result in severe cognitive deficits in choice, planning and executive processes. These cases make it clear that the capacity for goal-directed action is highly adaptive and studying animal models of these disorders forms an integral part of the approach we are taking to establishing the normal functioning of these systems. I am also interested in the psychological and neural determinants of reward, particularly establishing how these are distinguished from more fundamental reinforcement and motivational processes and the way in which specific corticostriatal circuits are integrated with reward and reinforcement processes. In this context, the way that the reward value of both achieved and anticipated events - involving the amygdala as well as the insular and orbitofrontal cortices - initiate goal-directed actions is of particular interest. Drug addiction may be an important example of the way pathology in circuitry mediating reward leads to a failure to establish behavioral control. We are investigating this suggestion but, rather than focusing on circuits mediating pathological drug seeking, we are investigating whether the acquisition, extinction and re-instatement of drug-seeking reflects drug-induced pathology in those neural circuits critical for exerting executive control over actions and that contributes to the inhibition of habitual strategies.
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