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Up-Regulation of Akt and Nav1.8 in BmK I-Induced Pain 被引量:2
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作者 Guokun Zhou Yunlu Jiao +5 位作者 You Zhou Shichao Qin Jie Tao Feng Jiang Zhi-Yong Tan Yong-Hua Ji 《Neuroscience Bulletin》 SCIE CAS CSCD 2018年第3期539-542,共4页
Dear Editor,As the key contributor to the rising phase of action potentials in dorsal root ganglion(DRG)neurons,voltagegated sodium channels(VGSCs)are important in physiological and pathological pain conditions.Fo... Dear Editor,As the key contributor to the rising phase of action potentials in dorsal root ganglion(DRG)neurons,voltagegated sodium channels(VGSCs)are important in physiological and pathological pain conditions.For instance,abnormal expression of VGSCs in DRG neurons is the 展开更多
关键词 Akt In Up-Regulation of Akt and Nav1.8 in bmk i-induced pain
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Activation of mammalian target of rapamycin contributes to pain nociception induced in rats by BmK I, a sodium channel-specific modulator 被引量:4
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作者 Feng Jiang Li-Ming Hua +5 位作者 Yun-Lu Jiao Pin Ye Jin Fu Zhi-Jun Cheng Gang Ding Yong-Hua Ji 《Neuroscience Bulletin》 SCIE CAS CSCD 2014年第1期21-32,共12页
The mammalian target of rapamycin (mTOR) pathway is essential for maintenance of the sensitivity of certain adult sensory neurons. Here, we investigated whether the mTOR cascade is involved in scorpion envenomation-... The mammalian target of rapamycin (mTOR) pathway is essential for maintenance of the sensitivity of certain adult sensory neurons. Here, we investigated whether the mTOR cascade is involved in scorpion envenomation-induced pain hypersensitivity in rats. The results showed that intraplantar injection of a neurotoxin from Buthus martensii Karsch, BmK I (10 pg), induced the activation of mTOR, as well as its downstream molecules p70 ribosomal S6 protein kinase (p70 S6K) and eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), in lumbar 5-6 dorsal root ganglia neurons on both sides in rats. The activation peaked at 2 h and recovered 1 day after injection. Compared with the control group, the ratios of p-mTOR/p-p70 S6K/p-4E- BP1 in three types of neurons changed significantly. The cell typology of p-mTOR/p-p70 S6K/p-4E-BP1 immuno-reactive neurons also changed. Intrathecal administration of deforolimus, a specific inhibitor of mTOR, attenuated BmK I-induced pain responses (spontaneous flinching, paroxysmal pain-like behavior, and mechanical hypersensitivity). Together, these results imply that the mTOR signaling pathway is mobilized by and contributes to experimental scorpion sting-induced pain. 展开更多
关键词 bmk I mTOR p70 ribosomal S6 protein kinase 4E-binding protein 1 pain dorsal rootganglion
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脊髓5-HT3A受体对BmK I诱发的大鼠炎性痛的影响(英文) 被引量:4
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作者 傅晋 焦云露 +1 位作者 李正威 吉永华 《生理学报》 CAS CSCD 北大核心 2015年第3期283-294,共12页
通过皮下注射BmK I能够建立新型大鼠疼痛模型。五羟色胺(5-HT)受体参与调控动物疼痛相关行为。本文旨在研究5-HT3受体调控BmK I诱发疼的潜在机制。应用动物行为学、RT-PCR、蛋白印迹等技术手段进行相关研究,得到如下结果:足底注射Bm... 通过皮下注射BmK I能够建立新型大鼠疼痛模型。五羟色胺(5-HT)受体参与调控动物疼痛相关行为。本文旨在研究5-HT3受体调控BmK I诱发疼的潜在机制。应用动物行为学、RT-PCR、蛋白印迹等技术手段进行相关研究,得到如下结果:足底注射BmK I(10μg)可诱导脊髓L4~L5段5-HT3A受体蛋白与m RNA表达增多,鞘内注射5-HT3A受体特异性拮抗剂ondansetron减少了自发痛反应,减弱了BmK I诱发的单侧热敏和双侧机械超敏;足底注射BmK I可能诱发了小胶质细胞的激活,且该效应能够被鞘内预注射ondansetron所逆转。脊髓L4~L5段5-HT3A受体主要表达于神经元,而不表达于小胶质细胞;另外,鞘内预注射ondansetron能够降低趋化因子CX3CL1与趋化因子受体CX3CR1在脊髓L4~L5段的表达水平。以上结果提示,5-HT3A受体信号通路与小胶质细胞激活共同参与BmK I诱发疼的起始与维持。神经元5-HT3A受体可能间接地通过CX3CL1参与与小胶质细胞间的"串话",CX3CL1参与调控BmK I诱导的痛觉超敏与敏化。 展开更多
关键词 bmk I诱发痛 5-HT3A受体 小胶质细胞 痛觉超敏与敏化
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