Temporal Changes of Astrocyte Activation and Glutamate Transporter‐1 Expression in the Spinal Cord After Spinal Nerve Ligation‐Induced Neuropathic Pain
Wei Wang, Wen Wang, Yayun Wang, Jing Huang, Shengxi Wu, Yun‐Qing Li
Abstract
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Wei Wang, Wen Wang, Yayun Wang, Jing Huang, Shengxi Wu, Yun‐Qing Li
Abstract
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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 (<3 days) and persistent (>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 down-regulation 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.
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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 (<3 days) and persistent (>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 down-regulation 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.
Key concepts: Neuropathic pain, Astrocyte, Glutamate receptor, Spinal cord, Neuroscience, Allodynia, Spinal nerve, Medicine