Acute epileptic seizures induced by the γ-aminobutyric acid (GABA) blocking chemoconvulsant pentylenetetrazole (PTZ) had already been shown to produce seizure-like discharges and network connectivity changes.3 But we can now move beyond this observation and start dissecting how different cell populations contribute to the brain-wide dynamics. Using a range of specifically engineered zebrafish lines with cell-type specific expression of fluorescent calcium indicators, Diaz Verdugo and colleagues demonstrate the dynamics of both neurons and glial cells during PTZ-induced seizures. They show that early after PTZ exposure, glial cells are already more synchronized than neurons. Synchronous activity of glial cells in this early stage is associated with a dampening of neuronal activity—suggesting, perhaps, that this glial cell activity dampens runaway neuronal activity bursts in the early phase following PTZ. However, this relationship drastically changes when the ictal activity generalizes. On generalization of the seizure, synchronized bursts of astrocytic activity precede neuronal ictal bursts by seconds. This temporal relationship, and some additional optogenetic validation experiments indeed suggest that synchronized bursts of glial cell activity may play a causative role in the transition toward a generalized epileptic seizure in this model.