Thrombin Facilitates Seizures through Activation of Persistent Sodium Current

Objective An epileptic seizure is frequently the presenting sign of intracerebral hemorrhage (ICH) caused by stroke, head trauma, hypertension and a wide spectrum of disorders. However the cellular mechanisms responsible for occurrence of seizures during ICH have not been established. During intracerebral bleeding, blood constituents enter the neuronal tissue and produce both an acute and delayed effect on brain functioning. Among the blood components only thrombin has been shown to evoke seizures immediately after entering brain tissue. In the present study we tested the hypothesis that thrombin increase neuronal excitability in the immature brain through alteration of voltage-gated sodium channels.