Astroglial cells, with their intricate interactions with the neural network, play a pivotal role in multiple brain processes. These range from maintaining metabolic homeostasis to regulating key aspects of brain development and fostering connectivity within neural circuits. Furthermore, accumulating evidence indicates that aberrant astroglial genetics and physiology contribute to the pathophysiology observed across diverse forms of epilepsy. Previously we demonstrated distinct spatiotemporal signal dynamics in neurons and astroglia during the transition from pre-ictal to ictal activity and photic stimulation in hyperexcitable networks. In pre-ictal periods neurons exhibited local synchrony and low level of activity, whereas astroglia exhibit global synchrony and high-level calcium signals anti correlated with neuronal activity. Generalized seizures, however, were marked by a massive release of astroglial glutamate as well as a drastic increase of astroglial and neuronal activity and synchrony across the entire brain. Knocking out astroglial glutamate transporters led to recurrent spontaneous seizures, accompanied with massive astroglial glutamate release, resembling a neonatal form of epileptic encephalopathy. Currently, we are using a combination of genetic and pharmacological approaches to perturb astroglial calcium and glutamate signalling, astroglial gap junctions, and glia-neuron interactions to further investigate their role in generation and spread of epileptic seizures across the brain, as well as to precisely target and disrupt them to reduce seizure susceptibility.