Neuroprotective effects of testosterone on dendritic morphology following partial motoneuron depletion: efficacy in female rats.
Neuroprotective effects of testosterone on dendritic morphology following partial motoneuron depletion: efficacy in female rats.
复制标题
睾酮对部分运动神经元耗竭后树突形态的神经保护作用：对雌性大鼠的功效。
DOI：
10.1016/j.neulet.2009.09.007
复制
发表时间：
2009
影响因子：
2.5
通讯作者：
Sengelaub,DaleR
中科院分区：
文献类型：
--
作者：
Wilson,RandallE;Coons,KellieD;Sengelaub,DaleR
运动神经元缺失是一个重要的医学问题，能够导致严重的运动障碍，甚至死亡。我们以前已经证明，运动神经元的部分耗竭诱导树突萎缩，在剩余的运动神经元，伴随着减少运动激活。用睾酮治疗雄性大鼠减弱部分运动神经元耗竭后的退行性变化。为了测试睾酮是否在雌性中具有类似的作用，我们研究了支配雌性大鼠四头肌肌肉的运动神经元的潜在神经保护作用。肌肉注射霍乱毒素结合皂草素选择性杀死运动神经元。同时，一些注射皂草素的大鼠被植入含有睾酮的植入物或不接受治疗。四周后，存活的运动神经元标记霍乱毒素结合HRP，和树突状乔木重建的三维。与正常女性相比，部分运动神经元耗竭导致剩余的四头肌运动神经元树突长度减少，睾酮治疗大大减弱了这种萎缩。这些研究结果表明，睾酮对男性和女性的形态具有神经保护作用，进一步支持睾酮作为神经治疗剂在受损神经系统中的作用。
Motoneuron loss is a significant medical problem, capable of causing severe movement disorders and even death. We have previously demonstrated that partial depletion of motoneurons induces dendritic atrophy in remaining motoneurons, with a concomitant reduction in motor activation. Treatment of male rats with testosterone attenuates the regressive changes following partial motoneuron depletion. To test whether testosterone has similar effects in females, we examined potential neuroprotective effects in motoneurons innervating muscles of the quadriceps of female rats. Motoneurons were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, some saporin-injected rats were given implants containing testosterone or left untreated. Four weeks later, surviving motoneurons were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in three dimensions. Compared to normal females, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons, and this atrophy was greatly attenuated by testosterone treatment. These findings suggest that testosterone has neuroprotective effects on morphology in both males and females, further supporting a role for testosterone as a neurotherapeutic agent in the injured nervous system.