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Neurological Studies of Rewards Processing In Major Depression

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This lecture is free to attend although registration is required. To register, and for more information, please visit:

As a satellite to the Clinical Neuroscience and Mental Health Symposium, Dr Wayne C Drevets, Senior Investigator and Chief of Sectioning on Mood and Anxiety Disorders for the National Institute of Mental Health in the USA , will be delivering the 2009 Paykel Lecture entitled “Neurological Studies of Rewards Processing In Major Depression” on the 28th September, 6:30 pm in the The Martin Cohen Lecture Theatre, Cancer Research UK, Cambridge Research Institute, The Lee Ka Shing Centre Cambridge Biomedical Campus (Addenbrooke’s Site) Robinson Way.

Coffee and biscuits will be available before the lecture, from 6.00 pm with a reception after the lecture with wine and canapes and an opportunity for you to meet Dr Drevets.

Talk Abstract: A deficit in central reward processing is thought to underlie the diminished ability of individuals with major depressive disorder (MDD) to derive pleasure from activities once deemed enjoyable. Notably, the corticolimbic networks shown to mediate and modulate the neural processing of reward and behavioral incentive in studies of experimental animals also have been implicated in the pathophysiology of MDD by data from neuroimaging and neuropathological studies. These networks involve the orbitofrontal cortex (OFC), amygdala, hippocampus and anatomically related areas of the striatum where reductions in grey matter volume and alterations in neurophysiological activity exist in some MDD subgroups. Using PET and fMRI imaging my colleagues and I investigated patterns of neural activity and dynamic neurotransmitter function within these circuits in depressed subjects as they performed reward processing tasks. While performing a monetary incentive delay (MID) task, depressed MDD subjects showed altered hemodynamic activity in the OFC , hippocampus, amygdala and accumbens, as they anticipated initiating behavioral responses aimed at acquiring rewards or avoiding losses. These physiological abnormalities were associated with impaired modulation of the behavioral response to changing incentive levels. Currently remitted subjects with MDD showed an abnormal diathesis to develop both this same behavioral pattern on the MID task and abnormal glucose metabolism in the OFC and accumbens area under catecholamine depletion. Converging with these data, depressed patients also showed abnormally reduced dopamine release during reward processing and reduced dopamine D1 receptor binding in the anteroventral striatum. The results of these studies will be integrated with relevant neurobiological data from preclinical studies into circuitry-based models that may elucidate the neural basis of the anhedonia, amotivation and mood-congruent processing biases manifest clinically in MDD .

Biosketch: Dr. Drevets, M.D. joined the Intramural Research Program of the National Institute of Mental Health in 2001, after serving on the Psychiatry Department faculties of the University of Pittsburgh School of Medicine for four years and the Washington University School of Medicine for nine years. Dr. Drevets received his M.D. degree from the University of Kansas, and completed residency training in psychiatry and post doctoral fellowship training in imaging sciences at Washington University. Dr. Drevets’ research focuses on applying positron emission tomography (PET) and magnetic resonance imaging (MRI) to characterize the pathophysiology of mood disorders.

This talk is part of the Clinical Neuroscience and Mental Health Symposium series.

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