本文選題：疼痛　切入點(diǎn)：N-甲基-D-天門冬氨酸　出處：《河北醫(yī)科大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

【摘要】：傳統(tǒng)觀念認(rèn)為，脊髓水平病理性疼痛的產(chǎn)生和維持完全是由神經(jīng)元介導(dǎo)的。膠質(zhì)細(xì)胞(星型膠質(zhì)細(xì)胞和小膠質(zhì)細(xì)胞)因不能進(jìn)行細(xì)胞間的突觸性信息傳遞而被認(rèn)為在病理性痛中不起作用。然而，最近研究表明脊髓后角膠質(zhì)細(xì)胞也參與病理性疼痛的產(chǎn)生和維持。例如，各種傷害性刺激，如皮下注射炎性物質(zhì)、神經(jīng)損傷、脊髓免疫激活物等都可激活脊髓膠質(zhì)細(xì)胞。激活的膠質(zhì)細(xì)胞可釋放一系列神經(jīng)活性物質(zhì)，如活性氧化產(chǎn)物、一氧化氮、花生四烯酸、白細(xì)胞三烯、前列腺素、興奮性氨基酸(Excitatory amino acids，EAA)、神經(jīng)生長因子等。激活的膠質(zhì)細(xì)胞還可釋放促炎性細(xì)胞因子如白細(xì)胞介素-1、白細(xì)胞介素-6、腫瘤壞死因子等。給予抑制膠質(zhì)細(xì)胞代謝的藥物如氟代檸檬酸或CNI-1493可以產(chǎn)生明顯的鎮(zhèn)痛作用。以上現(xiàn)象表明，脊髓膠質(zhì)細(xì)胞的活化在病理性痛和痛過敏的產(chǎn)生和維持中發(fā)揮重要作用。但傷害性刺激引起脊髓膠質(zhì)細(xì)胞激活的機(jī)制尚不清楚。 EAA是脊髓中傳遞傷害性信息的重要神經(jīng)遞質(zhì)。已有資料表明，N-甲基-D-天門冬氨酸(N-methyl-D-aspartic acid，NMDA)型EAA受體參與介導(dǎo)神經(jīng)病性疼痛模型中脊髓后角星型膠質(zhì)細(xì)胞的激活。但在外周炎性痛過程中脊髓星型膠質(zhì)細(xì)胞的激活是否也有NMDA受體的參與尚未見報(bào)道。 因此，本實(shí)驗(yàn)通過觀察NMDA受體非競爭性抑制劑
[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.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363;R402

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