Dheen S T, Tay S S, Wong W C
Department of Anatomy, Faculty of Medicine, National University of Singapore, Kent Ridge.
J Hirnforsch. 1994;35(2):253-62.
This study describes the ultrastructural changes in the cuneate nucleus of the streptozotocin-induced diabetic rats at 3, 6, 9, and 12 months post-induction. At 3 and 6 months, post-diabetes, a marked atrophy was observed in the myelinated axons. The atrophic axons showed delamination of myelin sheath, tightly arranged lamellar whorls, vesicular elements and degenerating debris within the electron-lucent axoplasm. At 9 and 12 months post-diabetes, a variety of dystrophic and degenerating axonal profiles and dendrites were seen in neuropil. The dystrophic axonal profiles containing tubulovesicular elements, slit-like clefts, vacuoles, swollen mitochondria, membranous and multigranular bodies appeared to be hypertrophied. The degenerating axon terminals contained swollen mitochondria and clustered spherical agranular vesicles in their electron-dense granular axoplasm. The degenerating dendrites were identified by the presence of swollen mitochondria, dilated ER in the electron-dense cytoplasm and they often formed the synaptic glomeruli with central axon terminals. Macrophages containing lipid bodies and electron-dense elements in their cytoplasm were in the process of phagocytosis. In all the time intervals studied, the somata appeared to be normal and the number of dystrophic and degenerating axonal profiles in the cuneate nucleus of diabetic rats was significantly increased in comparison with age-matched saline injected control rats.
本研究描述了链脲佐菌素诱导的糖尿病大鼠在诱导后3、6、9和12个月时楔束核的超微结构变化。糖尿病发生后3个月和6个月,观察到有髓轴突明显萎缩。萎缩的轴突表现为髓鞘分层、紧密排列的板层涡、电子透明的轴质内的囊泡成分和退化碎片。糖尿病发生后9个月和12个月,在神经毡中可见各种营养不良和退化的轴突轮廓及树突。含有微管泡成分、裂隙样间隙、空泡、肿胀线粒体、膜性和多颗粒体的营养不良性轴突轮廓似乎肥大。退化的轴突终末在其电子致密的颗粒状轴质中含有肿胀的线粒体和聚集的球形无颗粒囊泡。退化的树突通过肿胀的线粒体、电子致密细胞质中扩张的内质网来识别,它们常与中央轴突终末形成突触小球。细胞质中含有脂质体和电子致密成分的巨噬细胞正处于吞噬过程中。在所有研究的时间间隔内,神经元胞体似乎正常,与年龄匹配的注射生理盐水的对照大鼠相比,糖尿病大鼠楔束核中营养不良和退化的轴突轮廓数量显著增加。