In schizophrenia, hypofunction of the NMDA receptor may involve GABAergic interneurons, which would result in disturbed glutamatergic transmission [47]. Moreover, there is a decrease of glutamate receptor density on GABAergic interneurons [48]. The summary effect is the inadequate inhibition of glutamatergic neurons, observed in electroencephalography as disturbances of coherent neuronal oscillation at a rate below 0.1 Hz [49] and γ rhythms (25–100 Hz) in PFC [47,50,51,52]. This information noise negatively affects the concentration process and cognitive functions [53,54,55]. Furthermore it can promote hallucinations [56], delusions, and disturbances of the thinking processes and cognitive functions typical of acute psychosis. One of the causes of these pathological conditions is a dysfunction of default mode network (DMN), the “rest system’ of the brain, which should be switched off when working memory networks such as the external attention system (EAS) are activated [53]. In schizophrenia, DMN deactivation is impaired, increasing information noise, intensifying cognitive dysfunction [53,57] and general functioning problems [58].
