David Lodge (BVSc 1963) worked in University of Bristol as a surgeon and anaesthetist, before doctoral studies with Tim Biscoe on the neuropharmacology of amino acids (PhD 1974). During postdoctoral studies at the Australian National University with David Curtis FRS, he helped establish the role of glutamate as a central neurotransmitter and characterised its actions between AMPA, NMDA and kainate receptor subtypes. At the Royal Veterinary College, David linked his interests in anaesthesia and glutamate receptors by making the key discovery that the dissociative anaesthetics, ketamine and phencyclidine, selectively blocked NMDA receptors. He related NMDA antagonism to psychotomimetic effects. This provided a basis for the glutamate hypothesis of schizophrenia and redirected pharmaceutical search for schizophrenia therapies. David was recruited as a director of Eli Lilly’s neuroscience program, where he helped develop glutamate receptor approaches to brain diseases, resulting in clinical trials, e.g. for schizophrenia, some of which are ongoing. David’s current research concerns the mechanism of action of new ‘legal highs’ and the consequences of spontaneous mutations in glutamate receptors.
Research Fellow, Department of Physiology and Pharmacology, University of Bristol