Temporal changes of astrocyte activation and glutamate transporter-1 expression in the spinal cord after spinal nerve ligation-induced neuropathic pain

Temporal changes of astrocyte activation and glutamate transporter-1 expression in the spinal cord after spinal nerve ligation-induced neuropathic pain
复制标题

脊髓神经结扎引起的神经性疼痛后脊髓中星形胶质细胞活化和谷氨酸转运蛋白-1表达的时间变化

DOI:
10.1002/ar.20673
复制
发表时间:
2008-05-01
影响因子:
2
通讯作者:
Li, Yun-Qing
Li, Yun-Qing
中科院分区:
医学4区
文献类型:
--
作者:
Wang, Wei;Wang, Wen;Li, Yun-Qing

文献摘要

被引文献

相似文献

星形胶质细胞活化参与神经病理性疼痛。谷氨酸转运体1(glutamate transporter-1,GLT-1)是谷氨酸清除剂,仅在星形胶质细胞上表达,可能与星形胶质细胞活化有关。在本研究中,我们试图阐明星形胶质细胞活化和GLT-1表达的时间变化过程,以及它们之间的相关性诱导的神经病理性疼痛模型,即,脊神经结扎(SNL),其中迅速出现(21天)的机械异常性疼痛和热痛觉过敏。免疫荧光染色显示,GLT-1的表达只在大多数(不是所有)的星形胶质细胞,即使当GLT-1的表达达到高峰。GLT-1的表达呈现出一个有趣的双相变化,SNL后表达先上调后下调。我们的研究结果还表明,SNL诱导同侧脊髓背角星形胶质细胞的显着和长期(>21天)的激活。这些结果提示星形胶质细胞的活化、GLT-1表达的改变以及它们之间的潜在关系可能在神经病理性疼痛的诱导和/或维持中起关键作用。本研究结果为了解星形胶质细胞和GLT-1参与神经病理性疼痛的机制提供了新的线索。
Astrocyte activation is involved in the neuropathic pain. As a glutamate scavenger, the glutamate transporter-1 (GLT-1) is exclusively expressed on the astrocytes and probably correlates with astrocyte activation. In the present study, we attempted to clarify the temporal changing courses of astrocyte activation and GLT-1 expression, as well as their correlations induced by a neuropathic pain model, namely, spinal nerve ligation (SNL) in which rapidly appearing (21 days) mechanical allodynia and thermal hyperalgesia were presented. Immunofluorescent staining showed that GLT-1 was expressed exclusively in most (not all) of the astrocytes, even when the GLT-1 expression reached its peak. The expression of GLT-1 displayed an interesting biphasic change, with an initial up-regulation followed by a downregulation after SNL. Our results also demonstrated that SNL induced a marked and long-term (>21 days) activation of astrocytes in the ipsilateral spinal dorsal horn. These results suggest that astrocyte activation, the change of GLT-1 expression and the potential relationship between them might play key roles in the induction and/or maintenance of neuropathic pain. The present results provide novel clues in understanding the mechanisms underlying the involvement of astrocytes and GLT-1 in the neuropathic pain.