Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons.
Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons.
复制标题
睾丸激素对邻近运动神经元死亡后体细胞神经元的形态和功能的神经保护作用。
DOI：
10.1002/cne.21885
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发表时间：
2009-01-20
影响因子：
2.5
通讯作者：
Sengelaub, Dale R.
中科院分区：
文献类型：
--
作者：
Little, Christine M.;Coons, Kellie D.;Sengelaub, Dale R.
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。我们以前已经表明，部分耗尽运动神经元的性二态性，高度雄激素敏感的脊髓运动人群诱导树突状萎缩，在剩余的运动神经元，这种萎缩是减弱与睾酮治疗。为了测试睾酮是否在更典型的运动神经元中具有类似的作用，我们研究了支配股四头肌的运动神经元的潜在神经保护作用。肌内注射霍乱毒素结合皂草素可选择性地杀死支配股内侧肌的运动神经元。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。4周后，用霍乱毒素标记的HRP标记支配同侧股外侧肌的运动神经元，并三维重建树突状动脉。与完整的正常男性相比，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，睾酮治疗可减弱这种萎缩。为了检查诱导的树突状萎缩的功能后果，以及睾酮治疗的衰减，使用外周神经记录评估剩余的四头肌运动神经元的激活。部分运动神经元耗竭导致运动神经活动幅度降低，这些变化通过睾酮治疗而减弱，提供了与睾酮治疗对四头肌运动神经元形态的神经保护作用相关的功能。总之，这些研究结果表明，睾酮在高度雄激素敏感以及更典型的运动神经元群体中对形态和功能具有神经保护作用，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 or even death. We have previously shown that partial depletion of motoneurons from sexually dimorphic, highly androgen-sensitive spinal motor populations induces dendritic atrophy in remaining motoneurons, and this atrophy is attenuated by treatment with testosterone. To test whether testosterone has similar effects in more typical motoneurons, we examined potential neuroprotective effects in motoneurons innervating muscles of the quadriceps. Motoneurons innervating the vastus medialis muscle 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, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Compared to intact normal males, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons, and this atrophy was attenuated by testosterone treatment. To examine the functional consequences of the induced dendritic atrophy, and its attenuation with testosterone treatment, the activation of remaining quadriceps motoneurons was assessed using peripheral nerve recording. Partial motoneuron depletion resulted in decreased amplitudes of motor nerve activity, and these changes were attenuated by treatment with testosterone, providing a functional correlate to the neuroprotective effects of testosterone treatment on quadriceps motoneuron morphology. Together, these findings suggest that testosterone has neuroprotective effects on morphology and function in both highly androgen-sensitive as well as more typical motoneuron populations, further supporting a role for testosterone as a neurotherapeutic agent in the injured nervous system.
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影响因子：
4.7
作者：
Hammond, J;Le, Q;LeBlanc, A
通讯作者：
LeBlanc, A
影响因子：
5.1
作者：
BISBY, MA;TETZLAFF, W
通讯作者：
TETZLAFF, W
影响因子：
4.2
作者：
Fargo, Keith N.;Alexander, Thomas D.;Jones, Kathryn J.
通讯作者：
Jones, Kathryn J.
影响因子：
2.5
作者：
GOLDSTEIN, LA;SENGELAUB, DR
通讯作者：
SENGELAUB, DR
影响因子：
15.9
作者：
COGGESHALL, RE
通讯作者：
COGGESHALL, RE