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睾酮无法挽救幼鼠中因轴突切断诱导死亡的运动神经元。

Testosterone fails to rescue motoneurons from axotomy-induced death in young rats.

作者信息

Yu W H, Cao C G

机构信息

Department of Cell Biology and Anatomical Sciences, City University of New York Medical School, NY 10031.

出版信息

Neuroreport. 1992 Dec;3(12):1042-4. doi: 10.1097/00001756-199212000-00002.

Abstract

This study was undertaken to determine whether testosterone acting on muscle alone could enhance motoneuron survival after axotomy. Facial nerves were transected unilaterally in 10-day old rats in which androgen receptors were already present in skeletal muscle but not yet developed in motoneurons. Testosterone treatment lessened chromatolysis but failed to reduce neuronal loss which reached more than 50% 2 weeks postaxotomy. The inefficacy of testosterone was attributed to the death of motoneurons before they could re-establish synaptic contact with targets, thereby rendering target-derived trophic substances stimulated by testosterone unable to rescue motoneurons in a timely manner. The present finding is consistent with our hypothesis that functional neuromuscular connectivity is a prerequisite for testosterone to promote neuronal survival.

摘要

本研究旨在确定仅作用于肌肉的睾酮是否能增强轴突切断术后运动神经元的存活。在10日龄大鼠中单侧切断面神经,此时雄激素受体已存在于骨骼肌中,但运动神经元中尚未发育。睾酮治疗减轻了染色质溶解,但未能减少神经元损失,在轴突切断术后2周神经元损失超过50%。睾酮无效归因于运动神经元在能够与靶标重新建立突触联系之前死亡,从而使睾酮刺激的靶标衍生营养物质无法及时挽救运动神经元。本研究结果与我们的假设一致,即功能性神经肌肉连接是睾酮促进神经元存活的先决条件。

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