Smith S E, Meldrum B S
Department of Neurology, Institute of Psychiatry, London, U.K.
Eur J Pharmacol. 1990 Oct 2;187(1):131-4. doi: 10.1016/0014-2999(90)90350-f.
DL-beta-N-methylamino-alanine (DL-BMAA; 1-10 mumol 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 gamma-D-glutamylamino-methylsulphonate (gamma-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-alpha-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.
DL-β-N-甲基氨基丙氨酸（DL-BMAA；脑室内注射1-10微摩尔）在小鼠中诱发了一种综合征，包括共济失调、眼睑下垂、抓挠、跳跃、肌阵挛性抽搐、阵挛性肌肉痉挛和强直性惊厥，用D-（-）-4-（3-膦酰基-2-丙烯基）-哌嗪-2-羧酸盐（D-（-）-CPPene；腹腔注射）预处理或与γ-D-谷氨酰氨基甲基磺酸盐共同给药（γ-D-GAMS与DL-BMAA；脑室内注射）均对该综合征无影响。用1-（氨基苯基）-4-甲基-7,8-亚甲基二氧基-5H-2,3-苯并二氮杂䓬（GYKI 52466；静脉注射）预处理可降低DL-BMAA、红藻氨酸和RS-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（RS-AMPA；脑室内注射）所致阵挛性惊厥的发生率。这些结果表明，兴奋性氨基酸受体的AMPA/quisqualate亚型参与了急性BMAA毒性作用。
