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逆行运输减少导致薄束核轴突营养不良。电子显微镜和光学显微镜研究。

Diminished retrograde transport causes axonal dystrophy in the nucleus gracilis. Electron- and light-microscopic study.

作者信息

Yoshikawa H, Tarui S, Hashimoto P H

出版信息

Acta Neuropathol. 1985;68(2):93-100. doi: 10.1007/BF00688629.

Abstract

To examine a possible cause of axonal dystrophy in the nucleus gracilis, dorsal root ganglion (DRG) neurons of rats were investigated by means of electron-microscopic autoradiography and horseradish peroxidase (HRP) tracing method. Following injections of tritiated amino acids into the L6 and S1 DRG, labeling was observed on the initial and halfway developed dystrophic terminals in the ipsilateral gracile nucleus. However, no grains or few, if any, were found on the well developed huge dystrophic endings. Compared with the thoracic and upper lumbar DRG, a decrease in velocity and amount of retrograde HRP transport was demonstrated in the lower lumbar and sacrococcygeal DRG neurons, especially of large cell diameter, irrespective of age of rats. These findings led us to conclude that the axonal dystrophy reflects a state of an anterograde overtransport of the axoplasm caused by a diminished retrograde transport which is specific to lower lumbar and sacrococcygeal DRG large neurons.

摘要

为了研究薄束核中轴突营养不良的可能原因,采用电子显微镜放射自显影术和辣根过氧化物酶(HRP)追踪法对大鼠背根神经节(DRG)神经元进行了研究。向L6和S1背根神经节注射氚标记氨基酸后,在同侧薄束核中最初和发育中期的营养不良终末上观察到标记。然而,在发育良好的巨大营养不良终末上未发现银粒,或仅发现极少银粒。与胸段和上腰段背根神经节相比,不论大鼠年龄,下腰段和骶尾段背根神经节神经元,尤其是大直径细胞,其逆行HRP运输的速度和量均降低。这些发现使我们得出结论,轴突营养不良反映了一种由逆行运输减少导致的轴浆顺行过度运输状态,这种逆行运输减少是下腰段和骶尾段背根神经节大神经元所特有的。

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