Simson E L, Gold R M, Standish L J, Pellett P L
Science. 1977 Nov 4;198(4316):515-7. doi: 10.1126/science.910144.
Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced. Similar infusions into the caudal hypothalamus, believed to contain unmyelinated axons of passage that mediate satiety, failed to alter food intake or body weight. Histological examination of the affected tissue confirmed the behavioral evidence that suggests that this technique spares axons but destroys cell bodies. Infusion of several other amino acids also damaged neurons while sparing axons of passage.
向被认为含有介导饱腹感的神经元的下丘脑前部注入L-谷氨酸钠，会导致持续的食欲亢进和肥胖，这表明已经造成了脑部损伤。向被认为含有介导饱腹感的无髓鞘传导轴突的下丘脑后部进行类似的注入，并未改变食物摄入量或体重。对受影响组织的组织学检查证实了行为学证据，即该技术可使轴突免受损伤，但会破坏细胞体。注入其他几种氨基酸也会损伤神经元，同时使传导轴突免受损伤。
