Tang H W, Cassel G
Department of Biomedicine, Defense Research Establishment, Umeå, Sweden.
Toxicol Lett. 1998 Nov 12;99(3):169-73. doi: 10.1016/s0378-4274(98)00157-x.
Effects of soman on N-methyl-D-aspartate (NMDA) evoked [3H]norepinephrine (NE) release were examined in rat brain cortical slices. NMDA increased [3H]NE release in a concentration-dependent manner. Soman could inhibit the increase evoked by NMDA, but carbachol, an agonist of cholinergic receptor, could potentiate the increase evoked by NMDA. Atropine (a selective muscarinic antagonist) attenuated the release of [3H]NE induced by NMDA in the presence of carbachol or acetylcholine (ACh), but had no effect on the release of [3H]NE induced by NMDA alone. Both d-tubocurarine (an antagonist of nicotinic receptor) and atropine had no effect on the release of [3H]NE induced by NMDA in the presence of soman. These results suggested that soman has a direct action at non-cholinergic sites, probably at NMDA receptors.
在大鼠脑皮质切片中研究了梭曼对N-甲基-D-天冬氨酸(NMDA)诱发的[3H]去甲肾上腺素(NE)释放的影响。NMDA以浓度依赖的方式增加[3H]NE的释放。梭曼可抑制NMDA诱发的增加,但胆碱能受体激动剂卡巴胆碱可增强NMDA诱发的增加。阿托品(一种选择性毒蕈碱拮抗剂)在存在卡巴胆碱或乙酰胆碱(ACh)的情况下减弱了NMDA诱导的[3H]NE释放,但对单独由NMDA诱导的[3H]NE释放没有影响。筒箭毒碱(一种烟碱受体拮抗剂)和阿托品在存在梭曼的情况下对NMDA诱导的[3H]NE释放均无影响。这些结果表明,梭曼在非胆碱能部位有直接作用,可能作用于NMDA受体。