  We address a biophysical network dynamical model to study how the modulation
of dopamine (DA) activity and related N-methyl-d-aspartate (NMDA) glutamate
receptor activity as well as the emerging Pre-Frontal Cortex (PFC) functional
connectivity network (FCN) affect inhibitory cognitive function in
schizophrenia in an antisaccade task. The values of the model parameters and
the topology of the PFC-FCN were estimated by minimizing the differences
between simulations and the observed distributions of reaction times (RT)
during the performance of the antisaccade task in 30 patients with
schizophrenia and 30 healthy controls. We show that the proposed model
approximates remarkably well the predicted prefrontal cortical DA hypo-activity
and the related NMDA receptor hypo-function as well as the FCN dysconnection
pattern that are considered as the major etio-pathological hypotheses to
explain cognitive deficits in schizophrenia.
