Here, we investigate how pharmacological inhibition and gene deletion of sEH exerts neuroexcitatory modulation and neuroprotection against ischemic hypoxic brain injury by utilizing N-[2-[[(Hexahydro-2-oxo-1H-azepin-3-yl) amino] carbonyl] phenyl]-benzo[b] thiophene-2-carboxamide (ANA12), a selective TrkB inhibitor23, and focusing on the role of BDNF-TrkB signaling and glutamate receptors. Here, NTRK2 is linked to brain injury.