Chang L W, Wenger G R, McMillan D E
Environ Res. 1984 Jun;34(1):123-34. doi: 10.1016/0013-9351(84)90082-3.
Young C57BL/6N mice were injected (ip) with trimethyltin chloride at a dosage of 3.0 mg/kg body wt. Animals were sacrificed between 48 to 72 hr postinjection by means of intracardial perfusion of saline solution followed by 2.5% buffered glutaraldehyde. For light microscopy, the cords were further fixed in 10% buffered formalin and embedded in Paraplast. For electron microscopy, tissue samples were obtained from the cord levels at L1-L4, further fixed in glutaraldehyde and osmium tetroxide, and embedded in Epon. Chromatolytic and vacuolar changes involving neurons mainly in the medial and lateral motor nuclei of the anterior horns were observed. Electron microscopy revealed lysosomal accumulation and extensive dilatation of the cytoplasmic membrane systems (endoplasmic reticulum, Golgi complex). Large intraneuronal vacuoles were formed as a result of extensive intraneuronal edema. Progressive distention of the cytoplasmic membranes resulted in severe vacuolation, disintegration, and total breakdown of the neurons.
将年轻的C57BL/6N小鼠腹腔注射氯化三甲基锡，剂量为3.0毫克/千克体重。在注射后48至72小时之间，通过心脏内灌注生理盐水，随后灌注2.5%的缓冲戊二醛处死动物。用于光学显微镜观察的脊髓，进一步固定于10%的缓冲福尔马林中，然后包埋于石蜡中。用于电子显微镜观察的组织样本取自L1-L4节段的脊髓，进一步用戊二醛和四氧化锇固定，然后包埋于环氧树脂中。观察到主要在前角内侧和外侧运动核的神经元出现染色质溶解和空泡化变化。电子显微镜显示溶酶体聚集以及细胞质膜系统（内质网、高尔基体复合体）广泛扩张。广泛的神经元内水肿导致形成大的神经元内空泡。细胞质膜的渐进性扩张导致严重的空泡化、解体以及神经元的完全崩解。
