Although failure of GABAergic inhibition is a commonly hypothesized mechanism underlying seizure disorders, the series of events that precipitate a rapid shift from healthy to ictal activity remain unclear.Furthermore, the diversity of inhibitory animed aniflex complete interneuron populations poses a challenge for understanding local circuit interactions during seizure initiation.Using a combined optogenetic and electrophysiological approach, we examined the activity of identified mouse hippocampal interneuron classes during chemoconvulsant seizure induction in vivo.Surprisingly, synaptic inhibition from parvalbumin- (PV) and somatostatin-expressing (SST) interneurons remained intact throughout the preictal period and early ictal phase.
However, these two sources of inhibition exhibited cell-type-specific differences in their preictal firing patterns and sensitivity to input.Our findings suggest that the onset of ictal activity is not associated with loss of firing by these interneurons or a teal horse blanket failure of synaptic inhibition but is instead linked with disruptions of the respective roles these interneurons play in the hippocampal circuit.