and disease. Excessive activation of TrkB caused by status epilepticus promotes
development of temporal lobe epilepsy (TLE), revealing TrkB as a therapeutic target for
prevention of TLE. To circumvent undesirable consequences of global inhibition of TrkB
signaling, we implemented a novel strategy aimed at selective inhibition of the TrkB-
activated signaling pathway responsible for TLE. Our studies of a mouse model reveal that …