McCall A, Glaeser B S, Millington W, Wurtman R J
Neurobehav Toxicol. 1979 Winter;1(4):279-83.
Rats received 3H-mannitol, which marks the intactness of the blood-brain barrier, and 14C-glutamate or 14C-aspartate by intracardiac injection after oral gavage with water, monosodium glutamate, monosodium aspartate, or sodium chloride (doses equiosmolar to 4 g/kg monosodium glutamate). Thirty min later, various brain regions (e.g., cerebellum, cortex, hypothalamus, and striatum) were assayed for tritium and carbon-14. In most regions in most animals given monosodium glutamate or hypertonic saline, the level of the carbon-14 acidic amino acid tended to parallel the extent of damage incurred by the blood-brain barrier, as indicated by high levels of tritium-labelled mannitol. These data suggest that severe hyperosmolarity may be a prerequisite for monosodium glutamate to produce neurotoxic changes, and may explain why elective dietary consumption of enormous quantities of glutamate, by animals given free access to water, fails to induce brain lesions.
给大鼠经口灌胃水、味精、天冬氨酸钠或氯化钠（剂量与4 g/kg味精等渗）后，通过心内注射给予标记血脑屏障完整性的3H-甘露醇以及14C-谷氨酸或14C-天冬氨酸。30分钟后，对各个脑区（如小脑、皮质、下丘脑和纹状体）进行氚和碳-14含量测定。在大多数给予味精或高渗盐水的动物的大多数脑区中，碳-14酸性氨基酸的水平往往与血脑屏障受损程度平行，这可通过高含量的氚标记甘露醇来表明。这些数据表明，严重的高渗状态可能是味精产生神经毒性变化的先决条件，这或许可以解释为什么给动物自由饮水并选择性地大量食用谷氨酸时，却不会诱发脑损伤。
