We use multidisciplinary approaches to study the brain mechanisms for learning and motivation. We seek to understand these mechanisms in the normal brain and to apply this knowledge to understand neuropsychiatric disorders. 


We ask how do learning and motivation operate in the brain? Learning and motivation are central to our ability to flourish and succeed in the world. They form the fundamental building blocks of our cognition and emotion.

We seek to link psychological processes (attention, reward, fear, aversion, associative learning) to the activity of defined cells in defined neural circuits. We are interested in how these circuits give rise to normal psychological function and well-being, as well as how these circuits can go awry, thereby contributing to dysfunction in anxiety, post traumatic stress, addiction, and schizophrenia.

All of our work draws on the rich heritage of theory in the psychology of learning and motivation.  We have a variety of projects currently underway studying different aspects of these issues. Some specific projects are described below.


Understanding fear and anxiety 

  Sengupta et al. (2015). Using chemogenetic approaches to identify the brain mechanisms for matching fear to danger.

Sengupta et al. (2015). Using chemogenetic approaches to identify the brain mechanisms for matching fear to danger.

Our ability to use past experience to predict the future, and respond appropriately, is a signature of adaptive behavior. In the case of fear and anxiety this involves matching our level of fear to the danger posed by a situation. If the danger is low, then we should be less afraid but vigilant. If the danger is high (assault, trauma), then we should be more afraid and respond appropriately (avoid, escape, defend).

Central to this matching is our encoding of prediction error: the difference between the magnitude of threat we expect to occur and that which actually occurs. Learning from errors in our predictions about danger enables us to match our learning and responses precisely to the actual danger posed and reduce fear when danger has passed.

Normally, this matching is very precise. We accurately encode threats and regulate both our fear learning and fear responses accordingly. However, sometimes this matching can go awry: it can be difficult to suppress our fear and anxiety or difficult to accurately encode the threat and we generalise fear learning and responses to a variety of innocuous situations. Such disorders of fear and anxiety are remarkably common, affecting up to 28% of Australians across their lifespan, and they impose significant burdens on sufferers and their families.

We are interested in how the brain matches fear to danger. More specifically, we map the neural circuits encoding and signalling fear prediction errors and then we measure and manipulate activity in these circuits to understand the nature of the information conveyed.

We use this knowledge to understand the normal circuits in the human brain for fear and anxiety as well as to understand how these circuits become dysregulated during clinical anxiety such as post-traumatic stress.



Understanding relapse and promoting abstinence from drug taking

  Khoo et al. (2015). Prevention of relapse to alcohol seeking via optogenetic silencing of the striatopallidal pathway.

Khoo et al. (2015). Prevention of relapse to alcohol seeking via optogenetic silencing of the striatopallidal pathway.

Alcohol-use disorders and other drug addictions are chronically relapsing conditions, characterised by cycles of use, abstinence, and relapse. They impose significant burdens on users, their families, and communities via increased rates of physical and mental health problems, reduced productivity, and higher utilisation of health and social services. A key problem is their chronically relapsing nature. The majority of abstinent users relapse to drug use. Thus, a fundamental goal is preventing relapse because this improves the health of drug users and brings significant economic benefits to the broader community. 

Experimental psychology provides important insights into the factors that trigger relapse and also those factors that can act protectively to promote abstinence, hence identifying pathways to recovery. Research in the lab is directed towards using this knowledge to understand multiple aspects of drug addiction, relapse, abstinence, and recovery. We map the neural circuits that drive relapse and then we use a variety of techniques to manipulate these circuits. We also describe some of the the behavioural conditions that act during abstinence to reduce craving and drug seeking, and we use these same techniques to identify the neural circuits that mediate this abstinence.

More precisely, we are interested in understanding the roles of the major afferents (prefrontal cortex, basolateral amygdala, thalamus, ventral hippocampus) to the ventral striatum and the major outputs from the ventral striatum (pallidum, lateral hypothalamus, midbrain) in governing the balance between relapse and abstinence, and we study these pathways using a variety of approaches and techniques from modern neuroscience.



We have active collaborations with a number of colleagues inside and outside the School.

Within UNSW we collaborate with:

More broadly, we have active collaborations with:

  •  Associate Professor Elena Bagley (Pharmacology, School of Medical Sciences. University of Sydney) to study synaptic function in our fear and aversive learning projects
  • Dr John Power (Physiology, School of Medical Sciences, UNSW) to study synaptic function in our appetitive learning and drug seeking projects.
  • Associate Professor Pascal Carrive (School of Medical Sciences, UNSW) to study cardiovascular and autonomic function during fear and defense.

If you are interested in establishing a collaborative project then please contact Gavan.