DEGENERATION OF TRIGEMINAL GANGLION NEURONS CAUSED BY RETROGRADE AXONAL-TRANSPORT OF DOXORUBICIN
DEGENERATION OF TRIGEMINAL GANGLION NEURONS CAUSED BY RETROGRADE AXONAL-TRANSPORT OF DOXORUBICIN
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DOI：
10.1212/wnl.37.6.985
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发表时间：
1987-06-01
期刊：
影响因子：
9.9
通讯作者：
OLSSON, Y
中科院分区：
文献类型：
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作者：
BIGOTTE, L;OLSSON, Y
在小鼠三叉神经节中通过在头部的完整感觉神经末梢周围注射阿霉素（阿霉素）诱导选择性神经细胞变性。药物在神经分支中摄取后，明显通过逆行轴突运输到达神经元。直接荧光显微镜法显示，该化合物在神经元中积累。电子显微镜显示这些细胞的变性，从核仁和细胞核开始。在感觉神经末梢周围注射阿霉素似乎是用于选择性破坏小鼠感觉神经元的有用化合物。神经毒性化合物的轴突逆行转运可能是某些中毒形式的重要发病机制，引起神经系统的损害。
Selective nerve cell degeneration was induced in the trigeminal ganglion of the mouse by injecting doxorubicin (Adriamycin) around intact sensory nerve terminals of the head. The drug apparently reached the neurons by retrograde axonal transport after its uptake in nerve branches. A direct fluorescence microscopic method revealed that the compound accumulated in the neurons. Electronmicroscopy showed degeneration of these cells, beginning in the nucleolus and the nucleus. Doxorubicin injected around sensory nerve terminals appears to be a useful compound for selective destruction of mouse sensory neurons. Retrograde axonal transport of neurotoxic compounds is probably an important pathogenetic mechanism in certain forms of intoxication which give rise to lesions in the nervous system.