Over the past couple of decades, glial cells have been highlighted as active agents in hyperexcitability of neuronal networks, specifically playing key roles in seizure onset and termination. In particular, microglia have been suggested to have both neuroprotective and neurotoxic effects on the brain. Investigation into seizure termination is of particular interest, as it is sometimes followed by a postictal generalized EEG suppression (PGES) - a low activity state that is potentially associated with sudden unexpected death in epilepsy. In this study, we attempt to link glial effects - synaptic pruning and astrocytic potassium clearance - to the duration of spontaneous epileptiform discharges (SEDs) as well as interSED intervals (iSEDs). We build upon an earlier model of a neuroglial network by translating it into the cortical paradigm and including microglial units. Preliminary findings of our model demonstrated that the duration of SEDs is largely determined by the astrocytic potassium clearance, whereas iSEDs significantly increased with microglial-driven synaptic pruning. In our model, astrocytic potassium clearance itself did not bring a PGES-like state, whereas microglial effects did, which suggests a potential biomarker for PGES phenomena.