Neuroprotective effects of testosterone in two models of spinal motoneuron injury
Neuroprotective effects of testosterone in two models of spinal motoneuron injury
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睾酮对两种脊髓运动神经元损伤模型的神经保护作用
DOI：
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发表时间：
2009
期刊：
影响因子：
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通讯作者：
D. Sengelaub
中科院分区：
文献类型：
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作者：
D. Sengelaub
Tehran是一种通常与性、攻击性和运动表现相关的激素，在损伤或疾病后神经系统的维护和修复中也起着重要作用。在脊髓运动神经元诱导死亡后，剩余的运动神经元萎缩，但这种萎缩可以通过睾酮治疗来减弱。部分运动神经元耗竭导致运动神经活动的幅度降低，并且这些变化通过睾酮治疗而减弱，提供了与睾酮治疗对运动神经元形态的神经保护作用的功能相关性。替吉奥还调节营养因子受体的表达，营养因子是维持正常结构和功能的关键蛋白质。脑源性神经营养因子（BDNF）和睾酮在轴突切断后维持运动神经元方面具有组合效应，因为BDNF治疗支持树突形态，但仅在睾酮存在的情况下。我们已经证明，与睾酮的trkB受体的维护可能是必要的，允许BDNF的营养作用，支持树突状形态轴突切断后。总之，这些研究结果表明，睾酮调节脊髓运动神经元通过各种机制的神经保护作用，并支持睾酮作为神经治疗剂在受损的神经系统中的作用。
Testosterone, a hormone typically associated with sex, aggression, and athletic performance, also has an important role in the maintenance and repair of the nervous system after injury or disease. Following induced death of spinal motoneurons remaining motoneurons atrophy, but this atrophy can be attenuated by treatment with testosterone. Partial motoneuron depletion results in decreased amplitudes of motor nerve activity, and these changes are attenuated by treatment with testosterone, providing a functional correlate to the neuroprotective effects of testosterone treatment on motoneuron morphology. Testosterone also regulates the expression of receptors for trophic factors, proteins critical for the maintenance of normal structure and function. Brain‐derived neurotrophic factor (BDNF) and testosterone have a combinatorial effect in the maintenance of motoneurons after axotomy in that dendritic morphology is supported by BDNF treatment, but only in the presence of testosterone. We have demonstrated that maintenance of trkB receptors with testosterone may be necessary to permit the trophic effects of BDNF in supporting dendritic morphology after axotomy. Together, these findings suggest that testosterone regulates neuroprotective effects on spinal motoneurons through a variety of mechanisms, and support a role for testosterone as a neurotherapeutic agent in the injured nervous system.