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研究生:張靜嬋
研究生(外文):Ching-Tsan Chang
論文名稱:神經調節混合膠質細胞一氧化氮的分泌
論文名稱(外文):The regulation of NO secretion in glial cells by neurons
指導教授:吳劍男
指導教授(外文):Jian-Nan Wu
學位類別:碩士
校院名稱:國防醫學院
系所名稱:生理學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2003
畢業學年度:91
語文別:中文
論文頁數:84
中文關鍵詞:脂多醣體誘導型一氧化氮合成酶腎上腺素麩氨酸鹽
外文關鍵詞:LPSiNOSepinephrineglutamate
相關次數:
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在中樞神經系統之神經膠質細胞所分泌的一氧化氮扮演著免疫與媒介神經毒性作用的角色,能有產生發炎反應導致神經疾病。當膠質細胞給予內毒素脂多醣體刺激可產生不同的發炎調控物質,包括一氧化氮及細胞激素。本實驗主要目的是探討神經細胞對於脂多醣體刺激神經膠質細胞所產生一氧化氮之調控角色及其訊息傳遞路徑為何。利用神經膠質混合培養與膠質細胞相比較,發現有神經細胞之存在下,可減少脂多醣體所引發誘導型一氧化氮合成酶及一氧化氮之生成,但由神經原始細胞所分化的神經細胞則無法抑制膠質細胞的發炎反應。此結果未能進一步釐清細胞與細胞接觸的交互作用所扮演之角色。至於神經細胞所分泌的神經傳遞物質是否能抑制神經膠質細胞一氧化氮的釋放,研究結果發現少數神經傳遞物質如腎上腺素及麩氨酸鹽確實可抑制脂多醣體所引發的誘型一氧化氮合成酶及一氧化氮之生成,但其效力不如神經細胞。確實的機轉仍有待未來更進一步研究。由於腦部的發炎反應對於許多的神經疾病為重要的因素,因此本研究所提供有關於神經與膠質細胞之間對於發炎反應之交互影響,可以作為臨床治療神經退化性疾病之生理基礎。

Nitric oxide (NO) has been implicated in immune--mediated neurotoxicity in neuron-glia cultures and with various inflammation-related diseases in the CNS. When glial cells are exposed to endotoxins, such as the bacteria endotoxin lipopolysaccharide (LPS), it produced different inflammatory modulators, including NO and cytokines.This study aimed to elucidate the roles and mechanisms of neurons in modulating the production of NO in glial cells stimulated by LPS. Neurons with mixed glia showed reduced LPS-stimulated inducible NOS (iNOS) expression and nitrite production compared to mixed glia alone; Howerver, neurons developed from neural progenitor for cells would not do so.This results suggested that the influence of neurons on glial activation may not be attributed to the cell-cell interaction. Several neuron-secreted neurotransmitters can inhibit the release of NO in glia cells. we found that several neurotransmitters such as epinephrine and glutamate could partially inhibit LPS-induced iNOS expression and NO production,. Future studies are needed to uncover the mechanisms of this neuron-induced inhibition. Since cerebral inflammation is important in many neurological disorders, this study might provide insight about the role of neuron-glia interactions in inflammatory responses which may be fundamental to clinical therapy neurodegenerative disease.

目錄
                            頁次
目錄
圖次
中文摘要 I
英文摘要 II
第一章 緒論 1
第二章 實驗目的 14
第三章 材料與方法 15
第四章 結果 25
第五章 討論 31
第六章 結論 36
第七章 文獻參考 37
附圖 61

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