Please use this topic to ask questions about O3.
Changes in the chloride reversal potential most certainly happen during seizure, but from my reading they happen more during seizure propagation (i.e. after hyperactivity amongst interneurons has led to the necessary ion accumulations to trigger this change). Considering that, is it appropriate to model this change happening during inter-ictal discharges, before the seizure has started? (Disclaimer: I unfortunately missed the first 5 minutes or so of your talk so apologies if this was covered!)
We observed a shift of VGABA even in those slices that showed only interictal discharges (applied glutamatergic channel blockers and recorded evoked responses at different Vhold, in high-potassium solution). And generally, after application of proepileptic solution (with high potassium or just 4-AP), we observe first IID1s, which are pure GABAergic, and only later seizures emerge.
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