Lobner D, Lipton P
Department of Physiology, University of Wisconsin-Madison 53705.
Neurosci Lett. 1990 Sep 4;117(1-2):169-74. doi: 10.1016/0304-3940(90)90139-z.
Release of glutamate from brain cells is increased during ischemia and is thought to be involved in ischemic damage. In rat hippocampal slices the release of glutamate during 'in vitro ischemia' (anoxia without glucose) is shown to be blocked by two groups of compounds: non-competitive N-methyl-D-aspartate (NMDA) antagonists and sigma ligands. The effects are selective for the ischemic glutamate release, which is independent of extracellular Ca2+. High K+, Ca2+ dependent, induced release of glutamate is not inhibited. NMDA receptor blockade normally does not prevent ischemic transmission damage in the rat hippocampal slice. However, when ischemic glutamate release is attenuated, NMDA receptor antagonists do prevent the damage. This indicates that high levels of glutamate may cause damage via non-NMDA as well as NMDA receptors.
在缺血期间，脑细胞中谷氨酸的释放会增加，并且被认为与缺血性损伤有关。在大鼠海马切片中，“体外缺血”（无氧无糖）期间谷氨酸的释放被两类化合物所阻断：非竞争性N-甲基-D-天冬氨酸（NMDA）拮抗剂和西格玛配体。这些作用对缺血性谷氨酸释放具有选择性，其与细胞外Ca2+无关。高钾、Ca2+依赖性诱导的谷氨酸释放不受抑制。NMDA受体阻断通常不能防止大鼠海马切片中的缺血性传递损伤。然而，当缺血性谷氨酸释放减弱时，NMDA受体拮抗剂确实能防止损伤。这表明高水平的谷氨酸可能通过非NMDA受体以及NMDA受体导致损伤。
