Changes of amino acid levels and aspartate distribution in the cervical spinal cord after traumatic spinal cord injury.

Changes of amino acid levels and aspartate distribution in the cervical spinal cord after traumatic spinal cord injury.
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脊髓创伤后颈脊髓氨基酸水平和天冬氨酸分布的变化。

DOI:
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发表时间:
1998
影响因子:
4.2
通讯作者:
Y. Ogawa
Y. Ogawa
中科院分区:
医学2区
文献类型:
--
作者:
M. Watanabe;Y. Fujimura;M. Nakamura;Y. Yato;K. Ohta;H. Okai;Y. Ogawa

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为了评价兴奋性氨基酸在脊髓损伤后继发性损伤中的作用,迄今为止,已经进行了一些实验研究,重点是脊髓中氨基酸水平的变化。然而,由于技术的限制,它一直不可能与兴奋性氨基酸的总组织水平的兴奋性氨基酸的局部变化。为了研究损伤扩散与兴奋性氨基酸之间的联系,我们通过新的实验方法(如通过荧光显微光度法和组织病理学的免疫反应性)评估了天冬氨酸的局部变化,同时还通过HPLC分析了氨基酸的总组织水平。这些研究使用大鼠不完全颈脊髓损伤模型进行。通过这种方法,我们发现兴奋性氨基酸的水平,如谷氨酸和天冬氨酸,在损伤后立即开始下降。在其他氨基酸中未观察到显著降低。同样地,使用荧光显微光度法观察脊髓中天冬氨酸的局部变化。在前角和后角的减少是迅速的损伤后15分钟,但,此后放缓,这表明释放兴奋性氨基酸发生在原发性损伤后几乎立即受伤的网站。损伤后15分钟,损伤脊髓内的大神经元出现完整的组织病理学分析表明,兴奋性氨基酸的改变发生在组织病理学变化之前。白色物质的组织学变化比前角和后角慢,表明由于自碎机制引起的继发性损伤导致病变扩散。
To evaluate the role of excitatory amino acids in secondary injury occurring after spinal cord trauma, several experimental studies focusing on the the changes of amino acid levels in the spinal cord have been performed to date. However, because of technical limitations, it has not been possible to correlate the local changes of excitatory amino acids with the total tissue levels of excitatory amino acids. To investigate the connection between the spread of injury and the excitatory amino acids, we assessed, the local changes of aspartate through novel experimental approaches like immunoreactivity via fluorescence microphotometry and histopathology while also analyzing the total tissue levels of amino acids via HPLC. These studies were performed using a model of incomplete cervical spinal cord injury in rats. Through this approach, we found that the levels of excitatory amino acids, such as glutamate and aspartate, began to decrease immediately after injury. No significant decrease was observed in the other amino acids. Similarly, local changes in aspartate in the spinal cord were observed using fluorescence microphotometry. The decrease in the anterior and posterior horns was rapid up to 15 min after injury, but, slowed thereafter, suggesting that a release of excitatory amino acids occurred at the site of primary injury almost immediately following injury. At 15-min post-injury large neurons within the injured cord appeared intact on histopathological analysis demonstrating that the alteration of excitatory amino acids occurs prior to histopathological change. Histopathological change in the white matter occurred more slowly than in the anterior and posterior horns, suggesting the spread of the lesion by secondary damage due to an autoclastic mechanism.