L-β-甲基氨基丙氨酸诱导大鼠行为变化。

L-beta-methylamino-alanine-induced behavioral changes in rats.

作者信息

Matsuoka Y, Rakonczay Z, Giacobini E, Naritoku D

机构信息

Department of Pharmacology, Neurology, Southern Illinois University School of Medicine, Springfield 62794-9230.

出版信息

Pharmacol Biochem Behav. 1993 Mar;44(3):727-34. doi: 10.1016/0091-3057(93)90191-u.

DOI:10.1016/0091-3057(93)90191-u

PMID:8095728

Abstract

L-beta-N-methylamino-L-alanine (L-BMAA, 500 micrograms) infusions into the lateral ventricle induced splay, clonic convulsions, and rigidity in about 60% of rats. Electroencephalograph (EEG) recording during clonic convulsions and rigidity demonstrated epileptiform discharges. Duration and severity of L-BMAA-induced clonic convulsions were reduced significantly by DNQX, a non-NMDA glutamate receptor antagonist, but not by AP-5, a NMDA receptor antagonist or MK-801, a noncompetitive NMDA antagonist. Latency of L-BMAA-induced clonic convulsions was significantly prolonged by DNQX, AP-5 and MK-801. L-BMAA-induced splay was not modified by DNQX or AP-5 but was slightly enhanced by MK-801. L-BMAA-induced rigidity was abolished by MK-801 and partially inhibited by DNQX and AP-5. The L-BMAA-induced behaviors of grooming, facial tremor, etc. were affected by DNQX, AP-5, and MK-801. Our results suggest that L-BMAA may induce behavioral changes by acting upon several subtypes of excitatory amino acid receptors.

摘要

向大鼠侧脑室注射L-β-N-甲基氨基-L-丙氨酸（L-BMAA，500微克）可使约60%的大鼠出现伸展、阵挛性惊厥和强直。在阵挛性惊厥和强直发作期间进行脑电图（EEG）记录显示有癫痫样放电。非NMDA谷氨酸受体拮抗剂DNQX可显著降低L-BMAA诱导的阵挛性惊厥的持续时间和严重程度，但NMDA受体拮抗剂AP-5或非竞争性NMDA拮抗剂MK-801则无此作用。DNQX、AP-5和MK-801可显著延长L-BMAA诱导的阵挛性惊厥的潜伏期。DNQX或AP-5对L-BMAA诱导的伸展无影响，但MK-801可使其略有增强。MK-801可消除L-BMAA诱导的强直，DNQX和AP-5可部分抑制强直。L-BMAA诱导的梳理毛发、面部震颤等行为受DNQX、AP-5和MK-801的影响。我们的结果表明，L-BMAA可能通过作用于几种兴奋性氨基酸受体亚型来诱导行为改变。