- Christian Luscher, University of Geneva, Switzerland
Christian Lüscher is a neurologist & full professor of neuroscience at the University of Geneva. His research focuses on the neural basis of drug addiction.
During his training as a MD in Lausanne and Berne, he quantified the effects of axon morphology on action potential proportion in dorsal root ganglion cells. As a postdoctoral fellow at the University of California San Francisco from 1996-1999 his work concentrated on synaptic transmission and its plasticity.
With a career development award of the Swiss National Science Foundation he established his lab in Geneva, where he was appointed associate (2003) and then full professor (2009). During all these years he has maintained a clinical activity and is currently an attending in the HUG movement disorder clinic and member of the Geneva DBS team.
Christian Lüscher has published 60+ original articles that are cited more than 10’000 times. His core funding comes from the Swiss National Science foundation and the ERC (advanced grant 2013-9). His is a member of the senate of the Swiss Academy of Medical Sciences and the laureate of several prizes, including the Ott Prize (2017), the Koetzer Prize (2016) and the Cloëtta Prize (2010).
Scientific achievements include:
• Establishment of a classification of addictive drugs based on the cellular mechanism engaged by each substance to increase dopamine in the mesolimbic reward system.
• By systematical testing the hypothesis that altered synaptic transmission evoked by drugs underlies addictive behavior. This work has contributed to the emergence of a comprehensive circuit model of drug addiction and proposed a mechanism of individual vulnerability, a key question in the field.
• Translation of the circuit model for addiction into a novel deep brain stimulation (DBS) protocol that was successful in mice and is now tested in other species. The idea of optogenetically inspired DBS has been the focus of three international conferences that he chairs (OptoDBS).
• Investigation of feeding circuits that can override immediate metabolic needs. These projections partly overlap with addiction circuits and involve D1R expressing neurons from the nucleus accumbens to the lateral hypothalamus, which constitute a gate for food intake in the subsecond range. Similarly, afferents onto these accumbal neurons from the prefrontal cortex are undergoing synaptic plasticity when social cues between mice determines food preference.
« Go Back