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 in | Neuroscience letters Vol. 687; pp. 124 - 130 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier B.V
20.11.2018
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Online Access | Get full text |
ISSN | 0304-3940 1872-7972 1872-7972 |
DOI | 10.1016/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. |
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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 |
Author_xml | – sequence: 1 givenname: Hai-Feng surname: Lu fullname: Lu, Hai-Feng organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 2 givenname: Chun-Yang surname: Xu fullname: Xu, Chun-Yang organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 3 givenname: Lei surname: Zhang fullname: Zhang, Lei organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 4 givenname: Lei surname: Gan fullname: Gan, Lei organization: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 5 givenname: Chan surname: Chen fullname: Chen, Chan organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 6 givenname: Man-Yun surname: Yan fullname: Yan, Man-Yun organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 7 givenname: Xiao-Ning surname: Guo fullname: Guo, Xiao-Ning organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 8 givenname: Qi surname: Fang fullname: Fang, Qi organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 9 givenname: Guang-Yin surname: Xu fullname: Xu, Guang-Yin organization: Institute of Neuroscience, Soochow University, Suzhou 215123, China – sequence: 10 givenname: Yan-Bo surname: Zhang fullname: Zhang, Yan-Bo organization: Department of Neurology, Affiliated Hospital of Taishan Medical University, Taian 271000, China – sequence: 11 givenname: Jian-Qiang surname: Ni fullname: Ni, Jian-Qiang email: njq@suda.edu.cn organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China – sequence: 12 givenname: Hong-Ru surname: Zhao fullname: Zhao, Hong-Ru email: hongruzhao@suda.edu.cn organization: Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China |
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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 |
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