Androgenic, but not estrogenic, protection of motoneurons from somal and dendritic atrophy induced by the death of neighboring motoneurons

Androgenic, but not estrogenic, protection of motoneurons from somal and dendritic atrophy induced by the death of neighboring motoneurons
复制标题

DOI:
10.1002/dneu.20454
复制
发表时间:
2007-07-01
影响因子:
3
通讯作者:
Sengelaub, Dale R.
Sengelaub, Dale R.
中科院分区:
医学3区
文献类型:
--
作者:
Fargo, Keith N.;Sengelaub, Dale R.

文献摘要

被引文献

相似文献

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。我们一直在调查的影响,运动神经元的损失对存活的运动神经元在腰椎运动核,脊髓核的球海绵体肌(SNB)。SNB运动神经元经历显着的树突和体萎缩实验诱导死亡的其他附近的SNB运动神经元。然而,在损伤时用睾酮治疗可以减弱这种萎缩。由于睾酮可以代谢成雌激素雌二醇(以及其他生理活性类固醇激素),因此不知道睾酮的保护作用是雄激素效应,雌激素效应,还是两者兼而有之。在本实验中,我们使用了逆行运输的神经毒素杀死大多数的SNB运动神经元的脊髓一侧只在成年雄性大鼠。一些动物还接受睾酮、雄激素双氢睾酮(不能转化为雌二醇)或雌激素雌二醇治疗。如前所述,运动神经元部分缺失导致存活运动神经元的索马面积、树突长度和范围减少。睾酮和双氢睾酮减弱这些减少,但雌二醇没有保护作用。这些结果表明,睾酮对SNB运动神经元的形态学的神经保护作用部分运动神经元耗竭是雄激素效应,而不是雌激素效应。(c)2007 Wiley Periodicals,Inc.
Motoneuron loss is a significant medical problem, capable of causing severe movement disorders or even death. We have been investigating the effects of motoneuron loss on surviving motoneurons in a lumbar motor nucleus, the spinal nucleus of the bulbocavernosus (SNB). SNB motoneurons undergo marked dendritic and somal atrophy following the experimentally induced death of other nearby SNB motoneurons. However, treatment with testosterone at the time of lesioning attenuates this atrophy. Because testosterone can be metabolized into the estrogen estradiol (as well as other physiologically active steroid hormones), it was unknown whether the protective effect of testosterone was an androgen effect, an estrogen effect, or both. In the present experiment, we used a retrogradely transported neurotoxin to kill the majority of SNB motoneurons on one side of the spinal cord only in adult male rats. Some animals were also treated with either testosterone, the androgen dihydrotestosterone (which cannot be converted into estradiol), or the estrogen estradiol. As seen previously, partial motoneuron loss led to reductions in soma area and in dendritic length and extent in surviving motoneurons. Testosterone and dihydrotestosterone attenuated these reductions, but estradiol had no protective effect. These results indicate that the neuroprotective effect of testosterone on the morphology of SNB motoneurons following partial motoneuron depletion is an androgen effect rather than an estrogen effect. (c) 2007 Wiley Periodicals, Inc.