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DOI 10.1007/s10072-012-1100-3

Медицинская библиотека · Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012

Degeneration of peripheral nervous system in rats experimentally induced by methylmercury intoxication.

Cao Bingzhen, Lv Wei, Jin Shan, Tang Jigang, Wang Shuicai, Zhao Heling, Guo Hongwei, Su Jing, Cao Xia

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Аннотация

The objective of this study is to elucidate the primary action of methylmercury chloride (MMC) intoxication on peripheral nervous system. We chronologically observed the pathological changes of sciatic nerve, dorsal root ganglion (DRG) neurons, ventral and dorsal roots in rats given 4 mg/kg/day of MMC on consecutive days and killed on days 11, 15, 18 and 21. On day 11, an initial axonal degeneration of type B neuron occurred, predominantly in the distal portions of sciatic nerve. The DRG type A neuron was infiltrated by MRF-1-positive macrophages on day 11. Electron microscopy also demonstrated degenerated mitochondria in type A neuron. On day 21, most of type A neurons seemed to have disappeared. However, type B neurons were well preserved. Immunoblotting with monoclonal antibodies, P0 and neurofilament, demonstrated that both of proteins significantly decreases from day 15. In conclusion, these results indicate that the primary action on type A neuron is the neuron body that consequently results in an anterograde degeneration of nerve fibers, while the type B neuron degeneration occurs in a dying-back process in this subacute model. These findings suggest that the mechanisms involved in the degeneration induced by MMC vary and may depend on certain intrinsic factors peculiar to these neurons.

Для цитирования: Cao Bingzhen, Lv Wei, Jin Shan, Tang Jigang, Wang Shuicai, Zhao Heling, Guo Hongwei, Su Jing, Cao Xia. Degeneration of peripheral nervous system in rats experimentally induced by methylmercury intoxication.. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 2012. DOI: 10.1007/s10072-012-1100-3.

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