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NMDA受体参与介导大鼠蜜蜂毒炎性痛所致脊髓后角星型胶质细胞的激活

发布时间:2018-03-08 05:33

  本文选题:疼痛 切入点:N-甲基-D-天门冬氨酸 出处:《河北医科大学》2005年硕士论文 论文类型:学位论文


【摘要】:传统观念认为,脊髓水平病理性疼痛的产生和维持完全是由神经元介导的。胶质细胞(星型胶质细胞和小胶质细胞)因不能进行细胞间的突触性信息传递而被认为在病理性痛中不起作用。然而,最近研究表明脊髓后角胶质细胞也参与病理性疼痛的产生和维持。例如,各种伤害性刺激,如皮下注射炎性物质、神经损伤、脊髓免疫激活物等都可激活脊髓胶质细胞。激活的胶质细胞可释放一系列神经活性物质,如活性氧化产物、一氧化氮、花生四烯酸、白细胞三烯、前列腺素、兴奋性氨基酸(Excitatory amino acids,EAA)、神经生长因子等。激活的胶质细胞还可释放促炎性细胞因子如白细胞介素-1、白细胞介素-6、肿瘤坏死因子等。给予抑制胶质细胞代谢的药物如氟代柠檬酸或CNI-1493可以产生明显的镇痛作用。以上现象表明,脊髓胶质细胞的活化在病理性痛和痛过敏的产生和维持中发挥重要作用。但伤害性刺激引起脊髓胶质细胞激活的机制尚不清楚。 EAA是脊髓中传递伤害性信息的重要神经递质。已有资料表明,N-甲基-D-天门冬氨酸(N-methyl-D-aspartic acid,NMDA)型EAA受体参与介导神经病性疼痛模型中脊髓后角星型胶质细胞的激活。但在外周炎性痛过程中脊髓星型胶质细胞的激活是否也有NMDA受体的参与尚未见报道。 因此,本实验通过观察NMDA受体非竞争性抑制剂
[Abstract]:The conventional wisdom is that, The generation and maintenance of pathological pain at the spinal cord level is completely mediated by neurons. Glial cells (astrocytes and microglia) are thought to be involved in pathological pain because they are unable to transmit synaptic information between cells. It doesn't work. However, Recent studies have shown that glial cells in the posterior horn of the spinal cord are also involved in the generation and maintenance of pathological pain. For example, various noxious stimuli such as subcutaneous injection of inflammatory substances, nerve damage, The activated glial cells release a series of neuroactive substances, such as active oxidation products, nitric oxide, arachidonic acid, leukocyte triene, prostaglandin, etc. Excitatory amino acidsof EAA, nerve growth factor, etc. Activated glial cells can also release proinflammatory cytokines such as interleukin-1, interleukin-6, tumor necrosis factor, etc. Drugs that inhibit the metabolism of glial cells such as. Citric acid or CNI-1493 can produce obvious analgesic effect. The activation of spinal glial cells plays an important role in the production and maintenance of pathological pain and hyperalgesia, but the mechanism of nociceptive stimulation on the activation of spinal glial cells is unclear. EAA is an important neurotransmitter in the transmission of nociceptive information in the spinal cord. It has been reported that N-methyl-Daspartic acid (N-methyl-D-aspartic acid) type EAA receptor is involved in the activation of astrocytes in the spinal dorsal horn in a neuropathic pain model. Whether the activation of astrocytes in spinal cord is also involved in NMDA receptor during peripheral inflammatory pain has not been reported. Therefore, we observed the non-competitive inhibitor of NMDA receptor.
【学位授予单位】:河北医科大学
【学位级别】:硕士
【学位授予年份】:2005
【分类号】:R363;R402

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