[Seminar] "Is depression caused by a hyperactive habenula?", Prof. Jonathan Roiser

Dear all,

Neural Computation Unit (Doya Unit) would like to invite you to a seminar as follows.

Date: Tuesday, November 29, 2016
Time: 11:00-12:00
Venue: Meeting Room D015 - L1 Bldg
Speaker: Prof. Jonathan Roiser
Neuroscience and Mental Health at the UCL Institute of Cognitive Neuroscience (ICN), London
http://www.icn.ucl.ac.uk/Staff-Lists/MemberDetails.php?Title=Dr&FirstName=Jonathan&LastName=Roiser

Title: Is depression caused by a hyperactive habenula?

Abstract: A decade of research has revealed a key role for the habenula, a small structure adjacent to the thalamus, in the brain's processing of aversive stimuli. Not only does the habenula respond to such stimuli, it also inhibits midbrain dopamine neuron firing and its stimulation can drive conditioned place avoidance. Based on these findings, many investigators have suggested that habenula hyperactivity may play a role in depression, and this hypothesis is supported by work in animal models. However, the habenula hyperactivity hypothesis of depression has yet to be tested directly in humans, possibly due to the habenula's small size, which makes its measurement challenging.

I will present two studies, both of which use a basic computational approach to examine the role of the habenula in humans, and whether it is hyperactive in depression. The first study (Lawson et al 2014, PNAS) showed that in healthy volunteers the habenula responds to aversively conditioned stimuli in a manner consistent with learning. As initially neutral cues became increasingly associated with painful electric shocks, habenula activation increased significantly.  The second study (Lawson et al 2016, Molecular Psychiatry) showed a similar pattern in an independent sample of healthy volunteers. However, in unmedicated depressed patients habenula activation significantly decreased in response to increasing association with shocks, contradicting the hypothesis. Habenula resting-state perfusion and volume were similar between the groups, though the latter correlated negatively with anhedonic symptoms. These data suggest that the habenula does function abnormally in depression, but that the simple hyperactivity hypothesis is probably incorrect.

Bio: Jonathan Roiser is Professor of Neuroscience and Mental Health at the UCL Institute of Cognitive Neuroscience (ICN), London, where he directs the Cognitive Neuropsychiatry group, and a Wellcome Trust Senior Investigator. His research aims to understand the neurobiological basis of psychiatric symptoms, combining behavioural and psychopharmacological approaches with neuroimaging techniques and computational analysis. His current research focuses on understanding motivational dysfunction in depression. He studied Natural Sciences at Trinity College, Cambridge, as an undergraduate and remained there for his doctorate in the Department of Psychiatry, including a year spent at the National Institute of Mental Health (NIMH), USA. Following a post-doctoral appointment at the UCL Institute of Neurology he took up his current faculty position at the ICN. He was the recipient of the 2013 British Psychological Society’s Spearman Medal, the 2013 British Association for Psychopharmacology’s Senior Psychopharmacology Award and a Philip Leverhulme Prize in Psychology in 2015. His work has been funded by the Medical Research Council, the British Academy, the Brain and Behavior Research Foundation and the Wellcome Trust. He founded and co-directs two PhD schemes: the UCL-NIMH Joint Doctoral Training Program in Neuroscience (since 2008); and the UCL  4-year PhD Programme in Mental Health (since 2011).