Kataoka Y, Niwa M, Koizumi S, Watanabe S, Kouzuma M, Taniyama K
Department of Pharmacology 2, Nagasaki University School of Medicine, Japan.
Jpn J Pharmacol. 1992 Jun;59(2):247-50. doi: 10.1254/jjp.59.247.
The effects of nebracetam were investigated on N-methyl-D-aspartate (NMDA) receptor- and voltage-operated Ca2+ channels (VOCC)-mediated neural dysfunction by directly monitoring the real-time dynamics of dopamine released from rat striatal slices. Nebracetam (10(-5) and 10(-4) M) completely protected against striatal dopaminergic impairment induced by L-glutamate and NMDA, respectively. BAY K-8644-evoked striatal dysfunction was not blocked by nebracetam (10(-4) M). Therefore, nebracetam seems to produce a neuroprotective action by interacting, at least in part, with NMDA receptor-operated Ca2+ channels.
通过直接监测大鼠纹状体切片中多巴胺释放的实时动态，研究了奈非西坦对N-甲基-D-天冬氨酸（NMDA）受体和电压门控性Ca2+通道（VOCC）介导的神经功能障碍的影响。奈非西坦（10^(-5)和10^(-4) M）分别完全保护免受L-谷氨酸和NMDA诱导的纹状体多巴胺能损伤。奈非西坦（10^(-4) M）未阻断BAY K-8644诱发的纹状体功能障碍。因此，奈非西坦似乎至少部分通过与NMDA受体操纵的Ca2+通道相互作用而产生神经保护作用。
