首页> 外文期刊>Journal of Neurocytology: A Journal of Cellular Neurobiology >Long-term acrylamide intoxication induces atrophy of dorsal root ganglion A-cells and of myelinated sensory axons.
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Long-term acrylamide intoxication induces atrophy of dorsal root ganglion A-cells and of myelinated sensory axons.

机译:长期丙烯酰胺中毒可引起背根神经节A细胞和髓鞘感觉轴突萎缩。

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We have examined the effects of acrylamide on primary sensory nerve cell bodies and their myelinated axons in chronic acrylamide intoxication. The numbers and sizes of dorsal root ganglion cell bodies (L5) and myelinated nerve fibers were estimated with sterelogical techniques in severely disabled rats which had been treated with 33.3 mg/kg acrylamide twice a week for 7.5 weeks. There was no loss of dorsal root ganglion cells or myelinated nerve fibers in the roots, the sciatic nerve, sural nerve, and a tibial nerve branch. The mean perikaryal volume of A-cells was reduced by 20% (2P < 0.001) from 50000 microm(3) in controls (CV = 0.13) to 40000 microm(3) (0.12), whereas B-cell volume was unchanged. All size-frequency distribution curves of myelinated axon area of peripheral nerves and sensory roots were shifted to the left towards smaller values in rats exposed to acrylamide. In the L5 sensory root 3 mm from the ganglion, there was a significant reduction of mean cross sectional area of myelinated axons by 14% (2P < 0.05) from 7.6 microm(2) (0.11) in controls to 6.5 microm(2) (0.13) in intoxicated rats. The mean cross sectional area of myelinated sural nerve axons was reduced by 22% (2P < 0.001) from 8.6 microm(2) (0.08) in controls to 6.7 microm(2) (0.17) in intoxicated rats. We conclude that chronic intoxication with acrylamide leads to selective atrophy of type A dorsal root ganglion cell bodies and simultaneous atrophy along their peripheral axons, whereas neuronal B-cell bodies and motor axons are spared. It is suggested that the neuronal atrophy might well represent a defect of neurofilament synthesis and transport.
机译:我们已经检查了丙烯酰胺对慢性丙烯酰胺中毒的初级感觉神经细胞体及其髓鞘轴突的影响。采用立体学方法对严重残疾的大鼠进行背根神经节细胞体(L5)和有髓神经纤维的数量和大小的估计,该大鼠每周两次接受33.3 mg / kg丙烯酰胺治疗7.5周。根,坐骨神经,腓肠神经和胫神经支中的背根神经节细胞或有髓神经纤维没有丢失。从控制(CV = 0.13)的50000 microm(3)到40000 microm(3)(0.12),A细胞的平均周缘体积减少了20%(2P <0.001)。在暴露于丙烯酰胺的大鼠中,周围神经和感觉根的髓鞘轴突区域的所有大小-频率分布曲线都向左移动,向较小的值。在距神经节3 mm的L5感觉根中,髓鞘化轴突的平均横截面积从对照组的7.6 microm(2)(0.11)降低到6.5 microm(2)(14%)(2P <0.05)( 0.13)在醉酒的大鼠中。有髓大鼠的腓肠神经轴突的平均横截面积从对照组的8.6 microm(2)(0.08)降低了22%(2P <0.001)至6.7 microm(2)(0.17)。我们得出的结论是,用丙烯酰胺长期中毒会导致A型背根神经节细胞体选择性萎缩,并沿其周围轴突同时萎缩,而神经元B细胞体和运动轴突则得以幸免。提示神经元萎缩很可能代表了神经丝合成和运输的缺陷。

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