Tay S S, Wong W C
Department of Anatomy, Faculty of Medicine, National University of Singapore.
J Neurocytol. 1991 May;20(5):356-64. doi: 10.1007/BF01355532.
This study reports ultrastructural changes in the gracile nucleus of male Wistar rats after streptozotocin-induced diabetes. During the acute phase (3-7 days) degenerating electron-dense dendrites and axon terminals were dispersed in the neuropil. Degenerating dendrites were characterized by an electron-dense cytoplasm, swollen mitochondria, dilated endoplasmic reticulum and scattered ribosomes. Degenerating axon terminals were characterized by an electron-dense cytoplasm and clustering of small spherical agranular vesicles. Degenerating axon terminals may form part of a synaptic glomerulus with a central electron-dense dendrite, or they may form the central element of a synaptic glomerulus. These degenerating profiles were absent in the gracile nucleus of the 3 and 7 days insulin-treated post-streptozotocin rats. Macrophages were present in the neuropil and were in the process of engulfing neuronal elements. During the medium phase (1-6 months), most of the degenerating dendrites and axon terminals had been engulfed or removed by macrophages. During the late phase (9-12 months) a second wave of degeneration occurred in the gracile nucleus, similar to the acute phase. During the medium and late phases, dystrophic axonal profiles were also significantly increased in the rats after streptozotocin treatment. It is concluded that the ultrastructural changes observed in the gracile nucleus in the present study were the result of streptozotocin-induced diabetes rather than a toxic effect of streptozotocin, even in the acute phase.
本研究报告了链脲佐菌素诱导的糖尿病雄性Wistar大鼠薄束核的超微结构变化。在急性期(3 - 7天),变性的电子致密树突和轴突终末散布在神经毡中。变性树突的特征是细胞质电子致密、线粒体肿胀、内质网扩张和核糖体散在分布。变性轴突终末的特征是细胞质电子致密以及小的球形无颗粒小泡聚集。变性轴突终末可能与中央电子致密树突一起形成突触小球的一部分,或者它们可能形成突触小球的中央成分。在链脲佐菌素处理后3天和7天接受胰岛素治疗的大鼠的薄束核中不存在这些变性形态。巨噬细胞存在于神经毡中,并且正在吞噬神经元成分。在中期(1 - 6个月),大多数变性树突和轴突终末已被巨噬细胞吞噬或清除。在后期(9 - 12个月),薄束核中出现了第二波变性,类似于急性期。在中期和后期,链脲佐菌素处理后的大鼠中营养不良性轴突形态也显著增加。得出的结论是,本研究中在薄束核中观察到的超微结构变化是链脲佐菌素诱导的糖尿病的结果,而不是链脲佐菌素的毒性作用,即使在急性期也是如此。