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首页> 外文期刊>Brain research >Ultrastructural and morphometric alterations in the aortic depressor nerve of rats due to long term experimental diabetes: Effects of insulin treatment
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Ultrastructural and morphometric alterations in the aortic depressor nerve of rats due to long term experimental diabetes: Effects of insulin treatment

机译：长期实验性糖尿病引起的大鼠主动脉下垂神经的超微结构和形态变化：胰岛素治疗的效果

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摘要

Most of the reports about an altered baroreflex attribute this condition to the diabetic efferent neuropathy of the aortic depressor nerve (ADN) (afferent arm of the baroreflex less explored). We evaluated the ADN ultrastructural alterations caused by long term experimental diabetes and the effects of insulin treatment. Wistar rats (N=14) received a single intravenous injection of streptozotocin (40 mg/kg) 12 weeks before the experiment. Control animals (N=9) received vehicle (citrate buffer). Insulin treated animals (N=8) received a single subcutaneous injection of insulin daily. Under pentobarbital anesthesia the ADNs were isolated and had their spontaneous activity recorded. Afterwards, proximal and distal segments of the nerves were prepared for transmission electron microscopy study. Morphometry of the unmyelinated fibers was carried out with the aid of computer software. ADN of the diabetic animals showed axonal atrophy for myelinated fibers, with more pronounced alterations of the myelin sheath, such as myelin infolding and out folding, presence of myelin balls and very thin myelin sheath in relation to the axonal size, particularly for the small myelinated fibers becoming evident. No differences were observed in myelinated fiber number and their density, as well as on the fascicular area. Unmyelinated fiber number was significantly larger in the diabetic group while fiber diameter was significantly smaller compared to control. This result suggests axonal atrophy or, if associated to the larger number of fibers present in this group, could indicate fiber sprouting. These alterations were more evident in the distal segments of the nerves and were moderated by insulin treatment.
机译：关于压力感受器反射改变的大多数报道都将这种情况归因于糖尿病主动脉降压神经（ADN）的传出神经病变（压力感受器的活动臂未得到充分研究）。我们评估了长期实验性糖尿病引起的ADN超微结构改变以及胰岛素治疗的效果。实验前12周，Wistar大鼠（N = 14）接受单次静脉注射链脲佐菌素（40 mg / kg）。对照动物（N ＝ 9）接受媒介物（柠檬酸盐缓冲液）。胰岛素治疗的动物（N = 8）每天皮下注射胰岛素一次。在戊巴比妥麻醉下，分离出ADN并记录其自发活性。之后，准备神经的近端和远端以进行透射电子显微镜研究。未髓鞘纤维的形态测定借助于计算机软件进行。糖尿病动物的ADN显示髓鞘纤维的轴突萎缩，髓鞘的改变更为明显，例如髓鞘的折叠和向外折叠，相对于轴突的大小，存在髓鞘球和非常薄的髓鞘，特别是对于小的髓鞘纤维变得明显。在有髓纤维数量及其密度以及束状区域均未观察到差异。与对照组相比，糖尿病组的无髓纤维数量明显更大，而纤维直径明显较小。该结果表明轴突萎缩，或者如果与该组中存在的大量纤维相关，则可能表明纤维发芽。这些改变在神经末梢更明显，并通过胰岛素治疗得以缓解。

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