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We address a biophysical network dynamical model to study how the modulationof dopamine (DA) activity and related N-methyl-d-aspartate (NMDA) glutamatereceptor activity as well as the emerging Pre-Frontal Cortex (PFC) functionalconnectivity network (FCN) affect inhibitory cognitive function inschizophrenia in an antisaccade task. The values of the model parameters andthe topology of the PFC-FCN were estimated by minimizing the differencesbetween simulations and the observed distributions of reaction times (RT)during the performance of the antisaccade task in 30 patients withschizophrenia and 30 healthy controls. We show that the proposed modelapproximates remarkably well the predicted prefrontal cortical DA hypo-activityand the related NMDA receptor hypo-function as well as the FCN dysconnectionpattern that are considered as the major etio-pathological hypotheses toexplain cognitive deficits in schizophrenia.

A biophysical network model reveals the link between deficient  inhibitory cognitive control and major neurotransmitter and neural  connectivity hypotheses in schizophrenia