AbstractTwo non‐protein amino acids ofLathyrus sativus, β‐(isoxazoline‐5‐on‐2‐yl)‐alanine (BIA) and its higher homologue α‐amino‐γ‐Cisoxazoline‐5‐on‐2‐yl)‐alanine (ACI) were tested for excitotoxic potential. BIA (0.5‐2.0 mM) but not ACI (2.0 mM) produced a concentration‐dependent neurodegeneration in mouse cortical explants. The neuronal damage was prevented by the prior and simultaneous application of 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), indicating that it was mediated by non‐N‐methyl‐D‐aspartate type receptors. BIA (0,5‐2.0 mM) activated CNQX‐sensitive currents which were significantly smaller than those activated by 3‐N‐oxalyl‐L‐2,3‐diaminopropanoic acid (β‐ODAP) or α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐propionic acid (AMPA) in the majority of neurons. In a small number of cells, BIA (2 mM) produced currents which were similar in amplitude to those activated by β‐ODAP (50 μM). These results suggest thatLathyrus sativusplants engineered to block the synthesis of β‐ODAP may accumulate a neurotoxic precurs