Kim J P, Goldberg M P, Choi D W
Eur J Pharmacol. 1987 Jun 12;138(1):133-6. doi: 10.1016/0014-2999(87)90349-9.
(-)-Naloxone, 1 mM, partially reduced neuronal loss induced by exposure of murine cortical cell cultures to N-methyl-D-aspartate (NMDA) or quinolinate, but produced little or no attenuation of kainate or quisqualate neurotoxicity. Antagonism of NMDA neurotoxicity was (-)-naloxone concentration-dependent between 100 microM and 3 mM. (+)-Naloxone produced a slightly greater reduction of NMDA neurotoxicity, arguing against mediation by opioid receptors. Although this novel neuron-protective action of (-)-naloxone was weak, it may contribute to reported beneficial effects in CNS ischemia.
1毫摩尔的（-）-纳洛酮可部分减轻将小鼠皮质细胞培养物暴露于N-甲基-D-天冬氨酸（NMDA）或喹啉酸所诱导的神经元损失，但对 kainate 或 quisqualate 的神经毒性几乎没有或没有产生减弱作用。在100微摩尔至3毫摩尔之间，NMDA神经毒性的拮抗作用呈（-）-纳洛酮浓度依赖性。（+）-纳洛酮对NMDA神经毒性的降低作用稍大，这与阿片受体介导的作用相悖。尽管（-）-纳洛酮这种新的神经保护作用较弱，但它可能有助于中枢神经系统缺血中所报道的有益效果。
