RECEPTOR-SITE SPECIFICITY FOR THE ACUTE EFFECTS OF BETA-N-METHYLAMINO-ALANINE IN MICE

DL-β-N-methylamino-alanine (DL-BMAA; 1-10 μmol i.c.v.) in mice induced a syndrome of: ataxia, ptosis, scratching, jumping, myoclonic jerks, clonic muscle spasms and tonic seizure, which was unaffected by pretreatment with D(-)-4-(3-phosphonoprop-2-enyl)-piperazine-2-carboxylate (D(-)-CPPene; i.p.), or by co-administration of γ-D-glutamylamino-methylsulphonate (γ-D-GAMS with DL-BMAA; i.c.v.). Pretreatment with 1-(aminophenyl)-4- methyl-7,8-methylendioxy-5H-2,3-benzodiazepine (GYKI 52466; i.v.) decreased the incidence of clonic seizures for DL-BMAA, kainic acid and RS-α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (RS-AMPA; i.c.v.). These results suggest an involvement of the AMPA/quisqualate subtype of excitatory amino acid receptors in acute BMAA toxicity. © 1990.