Porcella A, Fage D, Voltz C, Carter C, Scatton B, Bartholini G
Synthélabo Recherche (L.E.R.S.), Bagneux, France.
Eur J Pharmacol. 1991 Jun 25;199(2):267-9. doi: 10.1016/0014-2999(91)90469-7.
The neurotoxic effects of intrastriatally administered N-methyl-D-aspartate (NMDA) (250 nmol), as measured by reductions in striatal choline acetyl transferase activity and by increased binding of the glial marker [3H]PK 11195 10 days later, were reduced by coinfusion of the irreversible ornithine decarboxylase inhibitor difluoromethylornithine (250 nmol) in the rat. The data suggest a crucial role for the polyamines in NMDA receptor-mediated neurotoxicity.
通过纹状体内注射N-甲基-D-天冬氨酸（NMDA，250纳摩尔）来测定其神经毒性作用，10天后，纹状体胆碱乙酰转移酶活性降低以及神经胶质标记物[3H]PK 11195的结合增加，在大鼠中通过共同注入不可逆的鸟氨酸脱羧酶抑制剂二氟甲基鸟氨酸（250纳摩尔）可减轻这种毒性作用。数据表明多胺在NMDA受体介导的神经毒性中起关键作用。
