Objective To investigate whether the kainate （KA） receptor subunit GluR6 is involved in the acute inflammatory pain. Methods Formalin was injected into the mucosa of rectum in Sprague-Dawley rats to induce visceral ...Objective To investigate whether the kainate （KA） receptor subunit GluR6 is involved in the acute inflammatory pain. Methods Formalin was injected into the mucosa of rectum in Sprague-Dawley rats to induce visceral pain. The antisense oligodeoxynucleotides （ODNs） of GluR6 were injected once per day for 3 d before formalin injection, after which GluR6 protein level was examined by immunoblotting method. The change of visceral pain was also investigated. Results The expression of GluR6 in the spinal cord of rats increased after the formalin injection. Moreover, pre-treatment of GluR6 antisense ODNs could suppress GluR6 expression in the spinal cord of rats and decrease the scores of visceral pain at 45 min following formalin injection. Conclusion Kainate receptor subunit GluR6 plays an important role in the visceral pain induced by injection of formalin into the wall of rectum. GluR6 may serve as a potential target for the treatment of acute inflammatory visceral pain.展开更多
Our previous study showed that when glutamate receptor （GluR）6 C terminus-containing peptide conjugated with the human immunodeficiency virus Tat protein （GluR6）-9c is delivered into hippocampal neurons in a brain...Our previous study showed that when glutamate receptor （GluR）6 C terminus-containing peptide conjugated with the human immunodeficiency virus Tat protein （GluR6）-9c is delivered into hippocampal neurons in a brain ischemic model, the activation of mixed lineage kinase 3 （MLK3） and c-Jun NH2-terminal kinase （JNK） is inhibited via GluR6-postsynaptic density protein 95 （PSD95）. In the present study, we investigated whether the recombinant adenovirus （Ad） carrying GluR6c could suppress the assembly of the GluR6-PSD95-MLK3 signaling module and decrease neuronal cell death induced by kainate in hippocampal CA1 subregion. A seizure model in Sprague-Dawley rats was induced by intraperitoneal injections of kainate. The effect of Ad- Glur6-9c on the phosphorylation of INK, MLK3 and mitogen-activated ldnase kinase 7 （MKK7） was observed with western immunoblots and immunohistochemistry. Our findings revealed that overexpression of GluR6c inhibited the interaction of GluR6 with PSD95 and prevented the kainate-induced activation of INK, MLK3 and MKK7. Furthermore, kainate-mediated neuronal cell death was significantly suppressed by GluR6c. Taken together, GluR6 may play a pivotal role in neuronal cell death.展开更多
目的通过比较常规开颅减压和控制减压两种不同手术减压方式对治疗兔重型颅脑外伤后急性颅内高压脑组织中海人藻受体亚基5(GluR5)和海人藻受体亚基6(GluR6)的表达水平及脑组织微观病理变化,探讨控制减压技术治疗重型颅脑伤的可能机制,为...目的通过比较常规开颅减压和控制减压两种不同手术减压方式对治疗兔重型颅脑外伤后急性颅内高压脑组织中海人藻受体亚基5(GluR5)和海人藻受体亚基6(GluR6)的表达水平及脑组织微观病理变化,探讨控制减压技术治疗重型颅脑伤的可能机制,为控制减压手术方法在临床应用提供理论依据。方法采用硬膜外球囊加压方法制备兔重型颅脑外伤后急性颅内高压的动物模型,新西兰白兔随机分为假手术组、控制减压组和常规减压组,观察术后24 h GluR5和GluR6的表达情况、术后兔脑组织HE染色、术后24 h ICP变化情况及术后兔头颅CT的变化。结果术后24 h,控制减压组GluR5的表达明显高于常规减压组(P<0.05),GluR6的表达明显低于常规减压组(P<0.05);脑组织HE染色控制减压组明显轻于常规减压组;控制减压组术后24 h ICP值明显低于常规减压组(P<0.05);控制减压组的脑梗塞发生率(10.5%)明显低于常规减压组(35.2%)(P<0.05)。结论控制减压模式治疗兔重型颅脑外伤能有效减轻脑缺血再灌注损伤(cerebral ischemia-reperfusion injury,I/R),降低术后脑梗塞等并发症发生率,起到明显的脑保护作用。展开更多
基金supported by the Natural Science Foundation of Jiangsu Province,China(No:BK2004028)
文摘Objective To investigate whether the kainate （KA） receptor subunit GluR6 is involved in the acute inflammatory pain. Methods Formalin was injected into the mucosa of rectum in Sprague-Dawley rats to induce visceral pain. The antisense oligodeoxynucleotides （ODNs） of GluR6 were injected once per day for 3 d before formalin injection, after which GluR6 protein level was examined by immunoblotting method. The change of visceral pain was also investigated. Results The expression of GluR6 in the spinal cord of rats increased after the formalin injection. Moreover, pre-treatment of GluR6 antisense ODNs could suppress GluR6 expression in the spinal cord of rats and decrease the scores of visceral pain at 45 min following formalin injection. Conclusion Kainate receptor subunit GluR6 plays an important role in the visceral pain induced by injection of formalin into the wall of rectum. GluR6 may serve as a potential target for the treatment of acute inflammatory visceral pain.
基金supported by the National Natural Science Foundation of China,No.30800309,81372172the Educational Science Foundation of Jiangsu Province,China,No.10KJB350005+2 种基金the Xuzhou Science Foundation in China,No.XZZD1153the President Special Grant of Xuzhou Medical College in China,No.09KJZ20a grant from the Zhenxing Project Foundation of XZMC
文摘Our previous study showed that when glutamate receptor （GluR）6 C terminus-containing peptide conjugated with the human immunodeficiency virus Tat protein （GluR6）-9c is delivered into hippocampal neurons in a brain ischemic model, the activation of mixed lineage kinase 3 （MLK3） and c-Jun NH2-terminal kinase （JNK） is inhibited via GluR6-postsynaptic density protein 95 （PSD95）. In the present study, we investigated whether the recombinant adenovirus （Ad） carrying GluR6c could suppress the assembly of the GluR6-PSD95-MLK3 signaling module and decrease neuronal cell death induced by kainate in hippocampal CA1 subregion. A seizure model in Sprague-Dawley rats was induced by intraperitoneal injections of kainate. The effect of Ad- Glur6-9c on the phosphorylation of INK, MLK3 and mitogen-activated ldnase kinase 7 （MKK7） was observed with western immunoblots and immunohistochemistry. Our findings revealed that overexpression of GluR6c inhibited the interaction of GluR6 with PSD95 and prevented the kainate-induced activation of INK, MLK3 and MKK7. Furthermore, kainate-mediated neuronal cell death was significantly suppressed by GluR6c. Taken together, GluR6 may play a pivotal role in neuronal cell death.
文摘目的通过比较常规开颅减压和控制减压两种不同手术减压方式对治疗兔重型颅脑外伤后急性颅内高压脑组织中海人藻受体亚基5(GluR5)和海人藻受体亚基6(GluR6)的表达水平及脑组织微观病理变化,探讨控制减压技术治疗重型颅脑伤的可能机制,为控制减压手术方法在临床应用提供理论依据。方法采用硬膜外球囊加压方法制备兔重型颅脑外伤后急性颅内高压的动物模型,新西兰白兔随机分为假手术组、控制减压组和常规减压组,观察术后24 h GluR5和GluR6的表达情况、术后兔脑组织HE染色、术后24 h ICP变化情况及术后兔头颅CT的变化。结果术后24 h,控制减压组GluR5的表达明显高于常规减压组(P<0.05),GluR6的表达明显低于常规减压组(P<0.05);脑组织HE染色控制减压组明显轻于常规减压组;控制减压组术后24 h ICP值明显低于常规减压组(P<0.05);控制减压组的脑梗塞发生率(10.5%)明显低于常规减压组(35.2%)(P<0.05)。结论控制减压模式治疗兔重型颅脑外伤能有效减轻脑缺血再灌注损伤(cerebral ischemia-reperfusion injury,I/R),降低术后脑梗塞等并发症发生率,起到明显的脑保护作用。
