Narita N, Hashimoto K, Iyo M, Minabe Y, Yamazaki K
Division of Cortical Function Disorder, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan.
Eur J Pharmacol. 1995 Oct 6;293(3):277-80. doi: 10.1016/s0922-4106(05)80055-0.
We studied the mechanism of antagonism of p-chloroamphetamine-induced neurotoxicity by dextromethorphan. The pretreatment with potent and selective sigma receptor ligands, 4-phenyl-4-(1-phenylbutyl)piperidine (4-PPBP) and N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-ethylamine monohydrochloride (NE-100), did not alter the reduction of 5-hydroxytryptamine and 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the cerebral cortex by repeated administration of p-chloroamphetamine. These results suggest that sigma receptors might not play a significant role in the antagonism of p-chloroamphetamine-induced neurotoxicity by dextromethorphan.
我们研究了右美沙芬对氯苯丙胺诱导的神经毒性的拮抗机制。用强效且选择性的西格玛受体配体4-苯基-4-(1-苯基丁基)哌啶(4-PPBP)和N,N-二丙基-2-[4-甲氧基-3-(2-苯乙氧基)苯基]乙胺盐酸盐(NE-100)进行预处理，并未改变反复给予对氯苯丙胺后大脑皮层中5-羟色胺、5-羟色胺和5-羟吲哚乙酸的减少情况。这些结果表明，西格玛受体可能在右美沙芬对氯苯丙胺诱导的神经毒性的拮抗作用中不发挥重要作用。
