Rabbit experimental sensory ataxic neuropathy: anti-GD1b antibody-mediated trkC downregulation of dorsal root ganglia neurons
Rabbit experimental sensory ataxic neuropathy: anti-GD1b antibody-mediated trkC downregulation of dorsal root ganglia neurons
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DOI：
10.1016/s0304-3940(98)00985-9
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发表时间：
1999-02-05
影响因子：
2.5
通讯作者：
Kanazawa, I
中科院分区：
文献类型：
--
作者：
Hitoshi, S;Kusunoki, S;Kanazawa, I
我们以前报道过神经节苷脂GD1b免疫诱导兔实验性感觉神经病变。病兔的主要病理改变是中央轴突延伸至脊髓背柱的初级感觉神经元变性。介导本体感觉的初级感觉神经元的缺失促使我们研究trkC在背根神经节（DRG）中的表达，因为这种类型的神经元被认为主要依赖于神经营养因子-3介导的trkC信号。Northern blotting分析显示，急性期病兔DRG中trkC的表达明显降低。该结果与病兔DRG中任何阶段均未见淋巴细胞浸润提示抗gd1b抗体介导的trkC表达下调可能是该实验性感觉共济失调神经病变的发病机制之一。1999爱思唯尔科学爱尔兰有限公司版权所有。
We previously reported experimental sensory neuropathy in rabbit induced by the immunization of ganglioside GD1b. The major pathological change in diseased rabbits was degeneration of primary sensory neurons with central axons extending to the dorsal column of the spinal cord. The loss of primary sensory neurons that mediate proprioceptive sensation prompted us to investigate the expression of trkC in dorsal root ganglia (DRG) because this type of neuron is thought depend mainly on neurotrophin-3-mediated trkC signaling. Northern blotting analysis revealed markedly reduced expression of trkC in DRG of diseased rabbits in acute phase. This result together with the absence of lymphocytic infiltration in DRG of diseased rabbits at any stage suggests the anti-GD1b antibody-mediated down regulation of trkC expression could be one of the pathogenesis of this experimental sensory ataxic neuropathy. (C) 1999 Elsevier Science Ireland Ltd. Ail rights reserved.