Richter A, Löscher W
Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Hannover, Germany.
Brain Res. 1997 Jan 16;745(1-2):336-8. doi: 10.1016/s0006-8993(96)01254-1.
The effects of dextromethorphan and its metabolite dextrorphan on severity of dystonia were examined in mutant dystonic hamsters, an animal model of idiopathic paroxysmal dystonia, in which recent examinations have shown antidystonic effects of selective N-methyl-D-aspartate (NMDA) receptor antagonists. Dextromethorphan and dextrorphan are non-competitive NMDA receptor antagonists which additionally exhibit affinity for sigma receptors. Dextrorphan (20 and 40 mg/kg i.p.) significantly retarded the progression of dystonia at the higher dose, whereas dextromethorphan (20, 40, 60 mg/kg i.p.) failed to exert any antidystonic effects even at high doses which caused severe effects. The lack of antidystonic efficacy of dextromethorphan may be related to its higher affinity to sigma receptors compared with dextrorphan.
在突变型肌张力障碍仓鼠（一种特发性阵发性肌张力障碍的动物模型）中研究了右美沙芬及其代谢产物右啡烷对肌张力障碍严重程度的影响，最近的研究表明选择性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂在该模型中有抗肌张力障碍作用。右美沙芬和右啡烷是非竞争性NMDA受体拮抗剂，此外还对σ受体具有亲和力。右啡烷（腹腔注射20和40mg/kg）在较高剂量时显著延缓了肌张力障碍的进展，而右美沙芬（腹腔注射20、40、60mg/kg）即使在引起严重效应的高剂量下也未发挥任何抗肌张力障碍作用。右美沙芬缺乏抗肌张力障碍疗效可能与其对σ受体的亲和力高于右啡烷有关。
