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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 潘建源(Chien-Yuan Pan) | |
| dc.contributor.author | Yong-Sheng Wang | en |
| dc.contributor.author | 王詠生 | zh_TW |
| dc.date.accessioned | 2021-06-16T09:32:32Z | - |
| dc.date.available | 2020-08-24 | |
| dc.date.copyright | 2020-08-24 | |
| dc.date.issued | 2020 | |
| dc.date.submitted | 2020-08-14 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/59672 | - |
| dc.description.abstract | 鋅離子失衡和谷氨酸引起的興奮毒性都會促使神經細胞死亡，並造成神經退化性疾病。許多報告顯示谷氨酸會提升胞內鋅離子濃度，但機制尚未明確。我們的過去結果顯示多巴胺會透過cAMP-NO訊息路徑促使金屬硫蛋白 (MTs) 釋放鋅離子，提高胞內鋅離子濃度。在這篇研究中，我們採用鋅離子影像技術探討谷氨酸如何提升初代培養大鼠胚胎皮質神經細胞的胞內鋅離子濃度，並探討鋅離子在神經發炎中的角色。對谷氨酸受體的活化劑與拮抗劑中，NMDA能提升胞內鋅離子濃度，然而NMDA受體 (NMDAR)、AMPA受體、鈣調蛋白 (CaM)、與神經一氧化氮合成酶 (nNOS) 的對應拮抗劑，都能抑制谷氨酸引發的胞內鋅離子濃度上升。且胞外鈣離子/鋅離子螯合劑乙二胺四乙酸 (EDTA) 也降低了谷氨酸引發的胞內鋅離子濃度上升。因此，谷氨酸引發的胞內鋅離子濃度上升可能依賴於經由NMDAR流入的鈣離子及後續造成的CaM、nNOS活化。TPEN，一種鋅離子螯合劑及MCC950，一種細胞焦亡路徑的抑制劑無法抑制谷氨酸引發的神經細胞死亡，但TPEN能降低谷氨酸引發的介白素-1β，一個神經發炎相關酵素的表現上升。此外谷氨酸處理也引發ZIP2，一種鋅離子運輸蛋白的表現。這些結果解釋谷氨酸透過NMDAR-CaM-nNOS級聯來提升胞內鋅離子濃度，且此級聯對神經發炎的活化非常重要。谷氨酸作為最重要的興奮性神經傳遞物，了解其如何調控鋅離子平衡及相關基因表現將為神經退化性疾病提供新的治療策略。 | zh_TW |
| dc.description.abstract | Both Zn2+ dyshomeostasis and glutamate-induced excitotoxicity can lead to neuronal cell death and cause neurodegenerative disorders. Several reports have shown that glutamate stimulation can elevate the intracellular Zn2+ concentration ([Zn2+]i) but the mechanism is not clear. Our previous results have shown that dopamine elevates [Zn2+]i through the cAMP-NO signaling pathway leading to the release of Zn2+ from metallothioneins (MTs). In this study, we adopted Zn2+ imaging technique to verify how glutamate elevates [Zn2+]i in primary-cultured rat embryonic cortical neurons and examined the possibility of the activation of neuroinflammation. Glutamate and NMDA, but not AMPA or kainate (KA), could elevate [Zn2+]i; antagonists against NMDA receptor (NMDAR), AMPA receptor, calmodulin (CaM), and neuronal nitric oxide synthase (nNOS) greatly suppressed the glutamate-induced elevation of [Zn2+]i. In addition, chelating the extracellular Ca2+ and Zn2+ by ethylenediaminetetraacetic acid (EDTA) also blocked the glutamate-induced elevation of [Zn2+]i. Therefore, it is possible that glutamate-induced elevation of [Zn2+]i is dependent on the Ca2+ influx through the NMDAR and further activation of CaM and nNOS. To examine the involvement of Zn2+ and pyroptosis in glutamate-induced neuron death, we pretreated the neuron with TPEN, a cell-permeable Zn2+ chelator, and MCC950, an inhibitor of NLRP3 in pyroptosis pathway. The results showed that TPEN and MCC950 did not inhibit glutamate-induced cell death but TPEN suppressed the glutamate-enhanced expression of IL-1β. Glutamate treatment also enhanced the expression level of ZIP2, a zinc transporter protein. These results illustrate that glutamate elevates the [Zn2+]i through the NMDAR-CaM-nNOS cascade, which is important for the activation of neuroinflammation. Glutamate is the most important excitatory neurotransmitter, understanding how it regulates the Zn2+ homeostasis and related gene expression will provide new therapeutic strategy against neurodegenerative disorders. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T09:32:32Z (GMT). No. of bitstreams: 1 U0001-1308202020405700.pdf: 2407837 bytes, checksum: 21917a84e72bcacabaec1f9cff9c1d04 (MD5) Previous issue date: 2020 | en |
| dc.description.tableofcontents | 致謝 i Abstract ii 摘要 iv 1. Introduction 1 1.1 Zinc 1 1.1.1 Zn2+ homeostasis 1 1.1.2 Zn2+ transporters 2 1.1.3 Pathways of [Zn2+]i elevation 3 1.1.4 Zinc and neurodegenerative disorders 4 1.2 Glutamate 4 1.2.1 Glutamate receptors 4 1.2.2 Glutamate and neurodegenerative disorders 5 1.3 Programmed cell death 6 1.3.1 Apoptosis 6 1.3.2 Necroptosis 6 1.3.3 Pyroptosis 7 1.4 Aims 7 2. Material and methods 9 2.1 Chemicals 9 2.2 Primary culture of rat embryonic cortical neurons 9 2.3 Zn2+/Ca2+ imaging 10 2.4 MTT assay 11 2.5 mRNA gene expression 11 2.5 Drug treatment 12 2.6. Data analysis 12 3. Results 14 3.1 Glutamate induces the elevation of [Zn2+]i in cultured rat embryonic cortical neurons. 14 3.2 Glutamate induces elevation of [Zn2+]i in a dose-dependent manner 15 3.3 DNQX and AP5 block the glutamate-induced elevation of [Zn2+]i 15 3.4 NMDA but not AMPA or KA elevates the [Zn2+]i 16 3.5 Agonists of mGluRs do not induce Zn2+ response 17 3.6 Co-application of AMPA and NMDA induce large Zn2+ response 17 3.7 nNOS inhibitors suppress the glutamate-induced elevation of [Zn2+]i 18 3.8 EDTA reduces the glutamate-induced elevation of [Zn2+]i 18 3.9 PKA inhibitor does not reduce the glutamate-induced elevation of [Zn2+]i 18 3.10 CaM antagonist suppresses the glutamate-induced elevation of [Zn2+]i 19 3.11 Agonists of iGluRs elevate [Ca2+]i 19 3.12 TPEN suppresses the glutamate-induced elevation of [Zn2+]i 19 3.13 TPEN and MCC950 do not rescue glutamate-induced neuron death 20 3.14 TPEN may reduce the glutamate-induced increment of IL-1β expression 20 3.15 Glutamate may enhance the expression of ZIP2 21 4. Discussion 22 5. Reference 25 6. Table and Figures 29 Table 1. PCR primers for pyroptosis 29 Table 2. PCR primers for zinc transporters 30 Figure 1. Glutamate elevates [Zn2+]i in primary cultured rat embryonic cortical neurons. 35 Figure 2. Glutamate-induced elevation of [Zn2+]i is dose-dependent in cultured cortical neurons. 37 Figure 3. DNQX and AP5 blocked the glutamate-induced elevation of [Zn2+]i. 39 Figure 4. NMDA but not AMPA or KA induces the Zn2+ response. 41 Figure 5. Agonist of mGluRs do not induce Zn2+ response. 43 Figure 6. Co-application of AMPA and NMDA induce large Zn2+ response. 45 Figure 7. nNOS inhibitors suppressed the glutamate-induced elevation of [Zn2+]i. 47 Figure 9. KT5720 does not reduce the glutamate-induced elevation of [Zn2+]i. 51 Figure 10. W7 suppresses the glutamate-induced elevation of [Zn2+]i in a dose-dependent manner. 53 Figure 11. Agonists of iGluRs elevate [Ca2+]i to a similar level 55 Figure 12. TPEN suppresses the glutamate-induced elevation of [Zn2+]i. 57 Figure 13. TPEN and MCC950 does not rescue glutamate-induced cell death. 59 Figure 14. TPEN pretreatment reduces the glutamate-enhanced expression of IL-1β. 61 Figure 15. Glutamate enhances the expression of ZIP2. 65 Figure 16. Overview of Zn2+ regulations in glutamate-stimulated neurons. 66 | |
| dc.language.iso | en | |
| dc.subject | 興奮毒性 | zh_TW |
| dc.subject | 谷氨酸 | zh_TW |
| dc.subject | 鋅離子 | zh_TW |
| dc.subject | 谷氨酸 | zh_TW |
| dc.subject | 興奮毒性 | zh_TW |
| dc.subject | 神經退化性疾病 | zh_TW |
| dc.subject | 細胞焦亡 | zh_TW |
| dc.subject | ZnT | zh_TW |
| dc.subject | ZIP | zh_TW |
| dc.subject | ZIP | zh_TW |
| dc.subject | ZnT | zh_TW |
| dc.subject | 細胞焦亡 | zh_TW |
| dc.subject | 鋅離子 | zh_TW |
| dc.subject | 神經退化性疾病 | zh_TW |
| dc.subject | pyroptosis | en |
| dc.subject | Zn2+ | en |
| dc.subject | glutamate | en |
| dc.subject | excitotoxicity | en |
| dc.subject | neurodegeneration | en |
| dc.subject | ZnT | en |
| dc.subject | ZIP | en |
| dc.subject | Zn2+ | en |
| dc.subject | glutamate | en |
| dc.subject | excitotoxicity | en |
| dc.subject | neurodegeneration | en |
| dc.subject | pyroptosis | en |
| dc.subject | ZnT | en |
| dc.subject | ZIP | en |
| dc.title | 谷氨酸在初代培養大鼠胚胎皮質神經細胞中引發胞內鋅離子濃度上升對神經細胞死亡之影響探討 | zh_TW |
| dc.title | Study the Effects of Glutamate-induced Elevation of [Zn2+]i on Neuronal Cell Death in Primary-Cultured Rat Embryonic Cortical Neurons | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 108-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 劉佩珊(Pei-Shan Liu),林崇智(Chung-Chih Lin) | |
| dc.subject.keyword | 鋅離子,谷氨酸,興奮毒性,神經退化性疾病,細胞焦亡,ZnT,ZIP, | zh_TW |
| dc.subject.keyword | Zn2+,glutamate,excitotoxicity,neurodegeneration,pyroptosis,ZnT,ZIP, | en |
| dc.relation.page | 66 | |
| dc.identifier.doi | 10.6342/NTU202003321 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2020-08-17 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 生命科學系 | zh_TW |
| 顯示於系所單位： | 生命科學系 | |
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