Pharmacological Reversal Of Cardiorespiratory Deficiency In The KCNA1-Null Model Of SUDEP
The two leading mechanisms for SUDEP are seizure-related cardiac and respiratory dysfunction. This research tests the ability of two clinically available drugs, flupirtine and fluoxetine, to prevent death in a well-characterized model of human SUDEP, the Kcna1 potassium channel knockout mouse, which exhibits severe seizures, brain-driven heart dysfunction, and premature death. Flupirtine belongs to a class of drugs called KCNQ openers, which we predict will protect against SUDEP by normalizing the interplay between brain and heart. Fluoxetine (better known as Prozac) prevents the brain’s reuptake of the neurotransmitter serotonin, which we predict will protect against seizure-associated respiratory arrest and SUDEP.