The role of selective SATB1 deletion in somatostatin expressing interneurons on endogenous network activity and the transition to epilepsy.

Somatostatin (SST) expressing interneurons are the second most abundant group of inhibitory neurons in the neocortex. They mainly target the apical dendrites of excitatory pyramidal cells and are implicated in feedforward and feedback inhibition. In the present study, we employ a conditional knockout mouse, in which the transcription factor Satb1 is selectively deleted in SST-expressing interneurons resulting to the reduction of their number across the somatosensory barrel field.