Dr. Vollenweider’s research interests encompasses the area of psychopathology, cognitive neuroscience, psychopharmacology, and neuroimaging to study the neurobiology of psychotic and affective disorders and to develop novel treatments for these disorders . His current research focuses on the identification of brain mechanisms, and particularly the role of the brain glutamate and serotonin systems involved the modulation of self, visual perception, cognitive and emotional processes and social interaction in normal waking states and the dysfunctions of these processes in psychiatric patients. Multiple approaches including measures of experimental psychology, information processing (e.g. PPI, p50, MMN), and brain imaging techniques (e.g. PET, fMRI, MRS) are used for studying these functions.

Under the umbrella of the Heffter Research Center (HRC)pharmacological and non-pharmacological-induced altered states of consciousness (ASC) in healthy human subjects are used as models to identify functional and neurochemical underpinnings of self, visual perception, emotional and cognitive processes, their regulation and interdependence as well as their implication for health and psychiatric disorders. In particular, the ketamine, psilocybin, and MDMA challenge models have been developed and applied over the last 20 years, and have been instrumental to further elucidate the role of NMDA and 5-HT2A/1A receptor functions in the pathophysiology of psychotic disorders and mood regulation. Such drug models in combination with information processing measures such as PPI, p50 and MMN have been shown to be a promising approach in elucidating neurophysiological markers that are associated with different domains of psychopathology or cognitive impairments. In addition, blockade of NMDA receptors by ketamine or activation of 5-HT2A receptors by psilocybin has also been shown to alter brain oscillations and to shift emotional processing from the negative to the positive in healthy human subjects. Understanding of the mechanism of the action of these compounds may be instrumental to further elucidate the rapid or putative long-term antidepressant effects of these compounds reported in depression and anxiety, and relevant to the development of novel treatments for these disorders.

To bridge the gap between preclinical and clinical research, we also aim further at developing new translational models to investigate clinically relevant drug effects in healthy human subjects rather than patients. The finding that healthy human subject with low baseline sensory gating capacity (e.g. PPI, p50) differentially respond to antipsychotic agents may provide such a model to search for neurophysiological and genetic biomarkers as well as pharmacological effects pertinent for psychotic and affective disorders.

Keywords, Methods

Cognitive Neuroscience
Model of psychosis
Emotion preocessing
glutamate, serotonin
PPI, p50, MMN

Research co-operations:

University of California, San Diego, USA
Department of Psychiatry
Prof. Dr. Mark Geyer

University of California, San Diego, USA
Department of Psychiatry
Prof. Dr. Martin Paulus

Yale School of Medicine, USA
Department of Psychiatry
Prof. Dr. John Krystal

University of Cambridge, Cambridge, GB
School of the Biological Sciences
Department of Experimental Psychology
Prof. Dr. Trevor Robbins

Wellcome Trust Centre for Neuroimaging, GB
Institute of Neurology, University College London
Prof. Dr. Karl Friston

Center for Radiopharmaceutical Science, Zurich, CH
ETH Zurich, PSI and USZ
Prof. Dr. Simon Ametamey

University Hospital Zurich, Zurich, CH
PET Center of the Clinic for Nuclear Medicine
Prof. Dr. med. dipl. Ing. Alfred Buck

University Zurich, Zurich, CH
Institute of Psychology, Section Neuropsychology
Prof. Dr. rer. nat. Lutz Jäncke

University Zurich, Zurich, CH
Institute for Empirical Research in Economics
Prof. Dr. Klaas Enno Stephan