Using a pentylenetetrazole (PTZ)-induced epileptic seizure animal model in vivo and electrophysiological techniques in in vitro 4-aminopyridine (4-AP; 100 μM) acute hippocampal slice epilepsy models, we revealed that NBP decreased neuronal hyperexcitability through postsynaptic GluA2-lacking calcium-permeable AMPA receptors (CP-AMPARs). The gene discussed is CP; the disease is Seizure.