P50 suppression is a sensory gating phenomenon where the EEG response to the second out of two auditory clicks is decreased in amplitude. Clinical studies have reported the magnitude of P50 suppression to be impaired in schizophrenia. Here, we used a network model of multicompartmental neurons to explore the mechanisms of P50 suppression deficits in schizophrenia. The model consisted of a population of pyramidal neurons interconnected with two interneuron populations: large basket cells and neurogliaform cells, where the latter activates GABAB-receptor mediated post-synaptic currents in its target neurons. The model allowed us to alter ion-channel conductances as suggested by post-mortem RNA expression data, namely, the CommonMind data, from the prefrontal cortices (PFC) and anterior cingulate cortices (ACC) of schizophrenia patients and healthy controls. When we altered the conductance of the ion channels implicated by genome-wide association studies according to these data, our model predicted a generic decrease in excitability in layer V pyramidal cells. The decreased sensory gating observed in schizophrenia is thought to be, at least partly, mediated by GABAB receptors targeting the pyramidal neurons. Here, we explore different mechanisms by which P50-suppression-like neural behaviour can be attained and how the decreased pyramidal cell excitability, orchestrated by altered expression of ion channels, affects this behaviour. We discuss our findings in light of clinical EEG data from psychiatric disorder patients and healthy controls.Acknowledgements: Research Council of Finland (358049)