Although clinical applications are still missing, there is growing evidence for an involvement of glutamatergic mechanisms in the pathophysiology of schizophrenia. In this symposium, leading experts in the field will present the current knowledge and discuss recent developments in psychiatric genetics, neuroimaging and neurophysiology. Dan Rujescu will present the recent largest genome wide association study of schizophrenia which has identified also glutamatergic genes. This talk will discuss the findings, and subsequent attempts to mine those findings for disease relevance. Andreas Meyer-Lindeberg will demonstrate translational neuroimaging of connectomic effects of glutamate antagonists. Combining methods from graph theory with pharmaco-fMRI in a translational (rats and humans) setting, it was found that dynamic network flexibility is altered in schizophrenia, related to genetic risk, and improved by NMDA receptor antagonism. Such drugs lead to less-integrated and more-segregated information processing that may underpin psychotogenic and antidepressant effects of NMDA antagonists. In his talk Christoph Mulert will present new empirical data demonstrating mechanistic insights about the role of neural oscillations in the gamma-band frequency range for normal auditory perception and the emergence of AVH in schizophrenia. Moreover, he will present new data how NMDA-receptor anatagonists influence these neurophysiological mechansims and are associated with alterations of auditory perception and the emergence of AVH. Jürgen Gallinat will present new evidence concerning glutamate-dopamine interaction using magnetic resonance spectroscopy (MRS) to measure absolute glutamate concentrations in prefrontal, striatal and hippocampal voxels and striatal presynaptic dopamine synthesis capacity using F-18-FDOPA PET. The current observations strengthen the view that therapeutic agents for schizophrenia should target the dopamine as well as the glutamate system.