The mechanisms by which glial cells could amplify neuronal signals remain to be seen, but potential mechanisms include modulation of neuronal glutamate excitation, alteration in extracellular K+ buffering, release of “gliotransmitters,” and more. Diaz Verdugo and colleagues’ work highlights the role of calcium mediated glial glutamate release that has been described previously in rodents.7 But there are other mechanisms through which glial cells shape neuronal dynamics—including regulation of extracellular potassium concentrations, pH, and neuronal energy metabolism.8 Biophysically inspired computational models of varying complexity have been used to expand the view on glial cell contribution to ictal dynamics,9 and more theoretical models have long emphasized the role of non-neuronal dynamics in seizures. But, so far compelling whole-brain data on which to test some of the resultant prediction has been scarce. However, this is about to change with many new zebrafish lines of genetic epilepsies arriving on the scene,10 and the incredible detail with which we can now image their brain dynamics across neurons and glial cells alike.