Wieloch T, Engelsen B, Westerberg E, Auer R
Neurosci Lett. 1985 Jul 4;58(1):25-30. doi: 10.1016/0304-3940(85)90323-4.
Unilateral ablations of the motor cortex were performed on rats. One to two weeks following the ablation they were subjected to 30 min of reversible insulin-induced hypoglycemic coma. The levels of glutamate, aspartate, gamma-aminobutyric acid (GABA), taurine, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and phosphocreatine (PCr) were determined in frozen tissue sections from the superior half of the caudate nucleus. The lesions induced a specific reduction in the levels of glutamate by approx. 10% in the dorsal caudate nucleus ipsilateral to the lesion, while no significant differences in the levels of aspartate, GABA, taurine, ATP, ADP, AMP or PCr were noted. Neuronal necrosis in the caudate nucleus in animals subjected to 30 min of insulin-induced hypoglycemic coma and one week recovery was assessed by light microscopy. Contralateral to the lesion, extensive neuronal necrosis, mainly affecting small and medium-sized neurons, was observed in the dorsal and lateral caudate nucleus. In the caudate ipsilateral to the lesion a complete amelioration of necrosis was noted in areas subjacent to the lesion. The data suggest that hypoglycemic brain damage is induced by excitotoxins such as glutamate or related compounds.
对大鼠进行了单侧运动皮层切除术。切除术后1至2周，使它们经历30分钟的可逆性胰岛素诱导的低血糖昏迷。测定了来自尾状核上半部分的冷冻组织切片中谷氨酸、天冬氨酸、γ-氨基丁酸（GABA）、牛磺酸、三磷酸腺苷（ATP）、二磷酸腺苷（ADP）、一磷酸腺苷（AMP）和磷酸肌酸（PCr）的水平。损伤导致损伤同侧背侧尾状核中谷氨酸水平特异性降低约10%，而天冬氨酸、GABA、牛磺酸、ATP、ADP、AMP或PCr水平未观察到显著差异。通过光学显微镜评估了经历30分钟胰岛素诱导的低血糖昏迷并恢复一周的动物尾状核中的神经元坏死情况。在损伤对侧，在背侧和外侧尾状核中观察到广泛的神经元坏死，主要影响中小型神经元。在损伤同侧的尾状核中，在损伤下方区域观察到坏死完全改善。数据表明，低血糖性脑损伤是由谷氨酸或相关化合物等兴奋性毒素诱导的。
