Satb2 ablation decreases PTZ-induced seizure susceptibility and pyramidal neuronal excitability.

Special AT-rich sequence-binding protein 2 (Satb2) is a transcriptional regulator and people with SATB2 mutation or duplication could display epilepsy. However, whether Satb2 is related with epilepsy and its mechanisms are largely unexplored. Here we found that the expression of Satb2 was decreased following the neuronal hyperactivities. Ablation of Satb2 in mice would decrease incidence and stage of seizure induced by intraperitoneal injection of pentylenetetrazol (PTZ). At cellular levels, we found pyramidal neuronal excitability and excitatory synaptic inputs in CA1 were decreased in Satb2 mutant mice. Taking together, we proved that deletion of Satb2 in mice increased PTZ seizure threshold probably by modulating neuronal excitability.