A new central post-stroke pain rat model: autologous blood injected thalamic hemorrhage involved increased expression of P2X4 receptor

•Behavioral analysis demonstrated that the CPSP animals displayed a significant decrease in mechanical allodynia threshold.•A significant increase in P2 × 4 receptors expression in microglia in thalamic peri-lesion tissues post-hemorrhage.•The mechanical allodynia in rats with CPSP were reversed by b...

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Published inNeuroscience letters Vol. 687; pp. 124 - 130
Main Authors Lu, Hai-Feng, Xu, Chun-Yang, Zhang, Lei, Gan, Lei, Chen, Chan, Yan, Man-Yun, Guo, Xiao-Ning, Fang, Qi, Xu, Guang-Yin, Zhang, Yan-Bo, Ni, Jian-Qiang, Zhao, Hong-Ru
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 20.11.2018
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ISSN0304-3940
1872-7972
1872-7972
DOI10.1016/j.neulet.2018.09.023

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Abstract •Behavioral analysis demonstrated that the CPSP animals displayed a significant decrease in mechanical allodynia threshold.•A significant increase in P2 × 4 receptors expression in microglia in thalamic peri-lesion tissues post-hemorrhage.•The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors.•A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics.•A significant decrease in P2 × 4 receptor expression after treatment with adrenergic antidepressants and antiepileptics. Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
AbstractList Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
•Behavioral analysis demonstrated that the CPSP animals displayed a significant decrease in mechanical allodynia threshold.•A significant increase in P2 × 4 receptors expression in microglia in thalamic peri-lesion tissues post-hemorrhage.•The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors.•A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics.•A significant decrease in P2 × 4 receptor expression after treatment with adrenergic antidepressants and antiepileptics. Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
Author Xu, Chun-Yang
Guo, Xiao-Ning
Xu, Guang-Yin
Fang, Qi
Chen, Chan
Gan, Lei
Zhang, Yan-Bo
Lu, Hai-Feng
Ni, Jian-Qiang
Zhao, Hong-Ru
Zhang, Lei
Yan, Man-Yun
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Keywords Central post-stroke pain
Autologous blood
P2X4
Language English
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Snippet •Behavioral analysis demonstrated that the CPSP animals displayed a significant decrease in mechanical allodynia threshold.•A significant increase in P2 × 4...
Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral...
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SubjectTerms Autologous blood
Central post-stroke pain
P2X4
Title A new central post-stroke pain rat model: autologous blood injected thalamic hemorrhage involved increased expression of P2X4 receptor
URI https://dx.doi.org/10.1016/j.neulet.2018.09.023
https://www.ncbi.nlm.nih.gov/pubmed/30267847
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