Gerald M C, Gupta T K
Psychopharmacology (Berl). 1977 Nov 24;55(1):83-6. doi: 10.1007/BF00432821.
The amphetamine isomers impair the rotarod performance of rats in a dose-related manner, with (+)-amphetamine approximately four-times as potent as its (-)-isomer. At a rotation speed of 4 rpm, 60 min after i.p. administration, the TD50 values (mg/kg) were: (+)-amphetamine, 24 (21.9-26.4) and (-)-amphetamine, 96 (76.3-118.4), with the curves not deviating from parallelism. Coadministration of the peripheral cholinesterase inhibitor neostigmine salicylate (0.005 mg/kg) attenuated (+)-amphetamine neurotoxicity [30 (26.4-34.1)]. These results, in conjunction with previously reported effects of the drug on isolated nerve-muscle preparations, suggest that the muscle weakness produced by high doses of amphetamine may result from inhibition of transmission at the neuromuscular junction.
苯丙胺异构体以剂量相关的方式损害大鼠的转棒试验表现，其中（+）-苯丙胺的效力约为其（-）-异构体的四倍。腹腔注射给药60分钟后，在4转/分钟的旋转速度下，半数中毒剂量（TD50）值（mg/kg）分别为：（+）-苯丙胺，24（21.9 - 26.4）；（-）-苯丙胺，96（76.3 - 118.4），且两条曲线不偏离平行性。同时给予外周胆碱酯酶抑制剂水杨酸新斯的明（0.005 mg/kg）可减弱（+）-苯丙胺的神经毒性[30（26.4 - 34.1）]。这些结果，结合先前报道的该药物对离体神经肌肉标本的作用，表明高剂量苯丙胺产生的肌无力可能是由于神经肌肉接头处传递受到抑制所致。
