Dow K E, Riopelle R J
Department of Pediatrics, Queens University, Apps Research Centre, Kingston General Hospital, Ontario, Canada.
Neuroreport. 1990 Oct;1(2):111-4. doi: 10.1097/00001756-199010000-00007.
N-methyl-D-aspartate (NMDA) produced dose dependent neurite growth from 8 day chick embryo sensory neurons in-vitro on a laminin substrate. NMDA-stimulated neurite growth was blocked by the competitive antagonist D-2-amino-5-phosphonovaleric acid (APV), by an antagonist of the glycine modulatory site kynurenate, and by the NMDA ion channel antagonist Mg2+. Ethanol blocked the NMDA-mediated neurotrophic effect in a manner that was additive with the effects of Mg2+, but non-additive with the inhibitory influences of APV and kynurenate. Thus the influences of ethanol were mediated at the NMDA receptor/modulatory site. These observations have implications for the understanding of adverse influences of ethanol on neuronal development and connectivity and on activity-dependent enduring changes in synaptic changes in synaptic function.
N-甲基-D-天冬氨酸(NMDA)在体外对铺有层粘连蛋白的8日龄鸡胚感觉神经元产生剂量依赖性的神经突生长。NMDA刺激的神经突生长被竞争性拮抗剂D-2-氨基-5-磷酸戊酸(APV)、甘氨酸调节位点拮抗剂犬尿烯酸以及NMDA离子通道拮抗剂Mg2+阻断。乙醇以一种与Mg2+的作用相加,但与APV和犬尿烯酸的抑制作用不相加的方式阻断NMDA介导的神经营养效应。因此,乙醇的影响是在NMDA受体/调节位点介导的。这些观察结果对于理解乙醇对神经元发育和连接以及对突触功能中依赖活动的持久突触变化的不利影响具有重要意义。