Dheen S T, Tay S S, Wong W C
Department of Anatomy, Faculty of Medicine, National University of Singapore.
J Anat. 1994 Jun;184 ( Pt 3)(Pt 3):615-23.
Ultrastructural and morphometric studies were undertaken on the hypothalamic supraoptic nucleus of streptozotocin-induced diabetic rats over a period of 1 y. At 3 d, a few dendrites showing electron-dense cytoplasm and dilated rER were dispersed in the neuropil among seemingly normal neuronal somata. At 1-6 months, the somata contained numerous vacuoles of various sizes which probably originated from fragmented and dilated rER. Numerous unidentifiable vacuolated and electron-dense neuronal profiles were also seen in the neuropil. At 9-12 months, the number of degenerating electron-dense axon terminals and dendrites was markedly increased in diabetic rats. Glial cells containing electron-dense debris in their cytoplasm were involved in phagocytosis. At all time intervals studied, the mean cross-sectional cell area and mean cross-sectional nuclear area of supraoptic nuclei neurons of diabetic rats were significantly increased in comparison with age-matched controls injected with normal saline. The causative factors for these changes are not clear. However, it is suggested that the osmotic stress caused by chronic dehydration in the diabetic animals may be partly or wholly responsible for these ultrastructural changes.
对链脲佐菌素诱导的糖尿病大鼠下丘脑视上核进行了为期1年的超微结构和形态计量学研究。在3天时,一些细胞质电子密度高且粗面内质网扩张的树突分散在神经毡中看似正常的神经元胞体之间。在1至6个月时,胞体含有许多大小各异的空泡,这些空泡可能起源于破碎和扩张的粗面内质网。在神经毡中还可见到许多无法识别的空泡化和电子密度高的神经元轮廓。在9至12个月时,糖尿病大鼠中退化的电子密度高的轴突终末和树突数量明显增加。细胞质中含有电子密度高的碎片的神经胶质细胞参与了吞噬作用。在所有研究的时间间隔内,与注射生理盐水的年龄匹配对照组相比,糖尿病大鼠视上核神经元的平均横截面积和平均横截面积核面积均显著增加。这些变化的致病因素尚不清楚。然而,有人认为糖尿病动物慢性脱水引起的渗透应激可能部分或全部导致了这些超微结构变化。