However, we admit that the extracellular registrations used in the present study do not provide a sufficient dataset to robustly distinguish between the two biophysical mechanisms contributing to the generation of discharges in the status epilepticus regime, including the considered processes of the synaptic resource exhaustion (Model 1) and the shunting effect of slow potassium channels (Model 2). Here, KCNA3 is linked to status epilepticus.