Major depressive disorder usually presents as a complex mixture of emotional, cognitive and somatic symptoms. Current treatments include both pharmacological and psychological approaches. However, a significant proportion of patients fail to respond and the disease can develop into a very severe and debilitating, treatment resistant disorder. Despite the availability of drug treatments for more than 60 years and extensive clinical and pre-clinical research, the underlying biology of depression remain elusive. Our work focuses on studies to try to understand how cognitive affective processes contribute to the disease and the actions of antidepressant drugs. This seminar will describe our work developing translational rat models of cognitive affective behaviour and discuss how ‘reverse translation’ was used to generate the methods. I will also discuss how we have used pharmacological and psychosocial manipulations of affective state to test the validity of the approach. The final part of the talk will discuss studies testing a novel hypotheses about the mechanisms of action and rate of onset of antidepressant drugs and, how this new information could be applied in the clinic to give more rapid onset and efficacious antidepressant therapy.
Emma completed her BSc(Hons) in Pharmacology in Bristol in 1995. Sponsored by the BBSRC and Knoll Pharmaceuticals, she completed a PhD in Psychopharmacology in Bristol supervised by Prof David Nutt, Dr Alan Hudson and Dr Helen Jackson. Following a five year teaching post, she was awarded an RCUK Academic Fellowship co-funded by the British Pharmacological Society Integrative Pharmacology Fund. As part of this Fellowship, Emma worked with Prof Robbins and Jeffery Dalley at the University of Cambridge, Experimental Psychology Department. Now based in Bristol’s School of Physiology and Pharmacology, and a Reader in Psychopharmacology, Emma’s research focuses on studies to investigate the neural and neurochemical mediators of normal cognitive and emotional behaviour and how these may be disrupted in psychiatric disorders such as depression, anxiety and addiction.