In this review the contributions of dopaminergic, glutamergic and GABAergic neuronal pathways to the pathophysiology of schizophrenia is discussed. Hypofunction of the N-methyl-D-aspartic (NMDA) receptor at a subpopulation of the cortical GABAergic interneuronsmay explain, at least in part, schizophrenia like symptoms. During development, NMDA receptor hypofunction at subpopulation of GABAergic interneurons is an important feature for developing the pathophysiology of schizophrenia. This subpopulation of GABA interneurons seems important for temporal control of cortical inhibition and the generation of synchronous oscillations, specifically at the gamma range. In schizophrenia these oscillations seem to be disturbed, and this disturbance may be underlying for many of the symptoms of the disease. Furthermore, the disturbances could be a downstream effect of NMDA receptor hypofunction in the cortical GABAergic interneurons.