Lincoln J, Loesch A, Burnstock G
Department of Anatomy and Developmental Biology, University College London, UK.
J Hirnforsch. 1989;30(4):425-35.
The ultrastructure of the hypothalamo-neurohypophysial system of rats was examined 8 weeks after streptozotocin-induction of type I diabetes. These studies provided evidence for numerous neuronal alterations to the hypothalamo-neurohypophysial system in streptozotocin-diabetic rats. Changes were observed in the somata, dendrites and axons of both the supraoptic and paraventricular nuclei as well as in axon profiles in the neurohypophysis. Many of these changes suggest an increased activity of the hypothalamo-neurohypophysial complex, with increased synthesis of neurohypophysial hormones in the hypothalamus together with depletion of neurosecretory granules in axons in the neurohypophysis. Some degenerative changes, however, were also observed. It is proposed that chronic dehydration and hypoxia in diabetes may contribute to the ultrastructural reorganization of the hypothalamo-neurohypophysial complex in streptozotocin-diabetic rats.
在链脲佐菌素诱导的 I 型糖尿病大鼠中,于诱导 8 周后检查下丘脑 - 神经垂体系统的超微结构。这些研究为链脲佐菌素诱导的糖尿病大鼠下丘脑 - 神经垂体系统中大量神经元改变提供了证据。在视上核和室旁核的胞体、树突和轴突以及神经垂体的轴突轮廓中均观察到变化。其中许多变化提示下丘脑 - 神经垂体复合体活性增加,下丘脑神经垂体激素合成增加,同时神经垂体轴突中的神经分泌颗粒减少。然而,也观察到一些退行性变化。有人提出,糖尿病中的慢性脱水和缺氧可能导致链脲佐菌素诱导的糖尿病大鼠下丘脑 - 神经垂体复合体的超微结构重组。