The regulation of NO secretion in glial cells by neurons
碩士 === 國防醫學院 === 生理學研究所 === 91 === 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)...
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ndltd-TW-091NDMC01160042016-06-22T04:20:05Z http://ndltd.ncl.edu.tw/handle/57227747801855559137 The regulation of NO secretion in glial cells by neurons 神經調節混合膠質細胞一氧化氮的分泌 Ching-Tsan Chang 張靜嬋 碩士 國防醫學院 生理學研究所 91 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. Jian-Nan Wu 吳劍男 2003 學位論文 ; thesis 84 zh-TW |
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碩士 === 國防醫學院 === 生理學研究所 === 91 === 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.
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author2 |
Jian-Nan Wu |
author_facet |
Jian-Nan Wu Ching-Tsan Chang 張靜嬋 |
author |
Ching-Tsan Chang 張靜嬋 |
spellingShingle |
Ching-Tsan Chang 張靜嬋 The regulation of NO secretion in glial cells by neurons |
author_sort |
Ching-Tsan Chang |
title |
The regulation of NO secretion in glial cells by neurons |
title_short |
The regulation of NO secretion in glial cells by neurons |
title_full |
The regulation of NO secretion in glial cells by neurons |
title_fullStr |
The regulation of NO secretion in glial cells by neurons |
title_full_unstemmed |
The regulation of NO secretion in glial cells by neurons |
title_sort |
regulation of no secretion in glial cells by neurons |
publishDate |
2003 |
url |
http://ndltd.ncl.edu.tw/handle/57227747801855559137 |
work_keys_str_mv |
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