Porcella A, Fage D, Voltz C, Bourdiol F, Benavides J, Scatton B, Carter C
Department of Biology, Synthelabo Recherche (LERS), Bagneux, France.
Neurol Res. 1992;14(2 Suppl):181-3. doi: 10.1080/01616412.1992.11740046.
N-Methyl-D-aspartate (NMDA) receptor activation selectively releases the polyamines spermine and spermidine from the rat striatum in vivo. The intrastriatal injection of spermine or spermidine is neurotoxic, but this toxicity is not blocked by MK-801 and unlikely to be mediated via the NMDA receptor. The neurotoxic effects of intrastriatally injected NMDA can, however, be reduced by polyamine synthesis inhibition with difluoromethylornithine. Alterations in polyamine metabolism in the ischaemic brain, although perhaps induced by NMDA receptor activation, may contribute to ischaemic cell loss via NMDA-independent mechanisms, possibly related to the diverse effects of polyamines on calcium homoeostasis and channel function.
N-甲基-D-天冬氨酸（NMDA）受体激活可在体内选择性地从大鼠纹状体释放多胺精胺和亚精胺。纹状体内注射精胺或亚精胺具有神经毒性，但这种毒性不能被MK-801阻断，且不太可能通过NMDA受体介导。然而，用二氟甲基鸟氨酸抑制多胺合成可减轻纹状体内注射NMDA的神经毒性作用。缺血性脑中多胺代谢的改变虽然可能由NMDA受体激活诱导，但可能通过NMDA非依赖机制导致缺血性细胞丢失，这可能与多胺对钙稳态和通道功能的多种作用有关。
