Experimental sensory neuropathy induced by sensitization with ganglioside GD1b
Experimental sensory neuropathy induced by sensitization with ganglioside GD1b
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DOI：
10.1002/ana.410390404
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发表时间：
1996-04-01
影响因子：
11.2
通讯作者：
Kanazawa, I
中科院分区：
文献类型：
--
作者：
Kusunoki, S;Shimizu, J;Kanazawa, I
用纯化GD1b免疫的6只家兔中有3只发生共济失调感觉神经病变。他们四肢摊开躺在地板上，动作笨拙；但肌肉力量、张力和浅表感觉似乎完好无损。坐骨神经运动传导检查正常。脊髓背柱、背根和坐骨神经均有轴突变性。背根神经节内部分神经细胞体变性消失。未见脱髓鞘病变或单核细胞浸润。其余3只免疫兔无临床症状，未见病理改变。只接种佐剂的对照组未出现临床症状和病理改变。6只经GD1b免疫的家兔血清中均产生抗GD1b抗体。单克隆抗gd1b抗体GGR12免疫染色约一半的兔初级感觉神经元。因此，由于抗体介导的初级感觉神经元损伤，GD1b致敏可能导致家兔的共济失调感觉神经病变。
Three of six rabbits immunized with purified GD1b developed ataxic sensory neuropathy. They laid on the floor with their limbs splayed out, and their movements were awkward; but muscle power, tonus, and superficial sensation appeared to be intact. Sciatic nerve motor conduction studies were normal. Axonal degeneration was present in the dorsal column of the spinal cord, in the dorsal roots, and in the sciatic nerve. Some of the nerve cell bodies in the dorsal root ganglia had degenerated and disappeared. No demyelinative lesions or mononuclear cell infiltrations were seen in those regions. No pathological changes were present in the other three immunized rabbits that showed no clinical symptoms. Control rabbits inoculated only with adjuvants showed neither clinical symptoms nor pathological changes. Anti-GD1b antibody was raised in the sera from all six rabbits immunized with GD1b. The monoclonal anti-GD1b antibody GGR12 immunostained about one-half the rabbit primary sensory neurons. Sensitization with GD1b, therefore, may cause ataxic sensory neuropathy in rabbits due to antibody-mediated damage to the primary sensory neurons.