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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 潘建源 | zh_TW |
| dc.contributor.advisor | Chien-Yuan Pan | en |
| dc.contributor.author | 洪茂庭 | zh_TW |
| dc.contributor.author | Mao-Ting Hung | en |
| dc.date.accessioned | 2023-08-09T16:44:26Z | - |
| dc.date.available | 2023-11-09 | - |
| dc.date.copyright | 2023-08-09 | - |
| dc.date.issued | 2023 | - |
| dc.date.submitted | 2023-07-25 | - |
| dc.identifier.citation | Allan, S. M., Tyrrell, P. J., & Rothwell, N. J. (2005). Interleukin-1 and neuronal injury. Nature reviews. Immunology, 5(8), 629–640.
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Interleukin-1beta regulation of N-type Ca2+ channels in cortical neurons. Neuroscience letters, 403(1-2), 181–185. Zybura, A., Hudmon, A., & Cummins, T. R. (2021). Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability. Cells, 10(7), 1595. 何祐豪 (民 108)。探討NLRP3-Caspase 1 機制在鋅離子引發大鼠初代培養神經元死亡的角色。國立臺灣大學生命科學系，臺北市。 高陵 (民 111)。研究白介素-1β刺激提升初代培養大鼠胚胎皮質神經細胞胞內鈣離子濃度的訊息途徑。國立臺灣大學生命科學系，臺北市。 曾惠群 (民 108)。探討鋅離子在多巴胺誘導對大鼠初代培養神經細胞焦亡中的影響。國立臺灣大學生命科學系，臺北市。 | - |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/88365 | - |
| dc.description.abstract | 介白素-1β (IL-1β) 是免疫反應的發炎前期細胞激素 (proinflammatory cytokines) 之一，且為許多神經疾病及退化的指標。IL-1β 的典型訊息路徑是與其受體蛋白 IL-1R1 結合，活化下游骨髓分化初級反應蛋白 88 (MyD88)，進而透過轉錄因子 NF-κB，啟動發炎相關基因的表現。因此多數關於 IL-1β 的研究，多著重於長期處理對細胞活性的影響，但對於 IL-1β 對神經傳導的立即影響及機制則了解較少。在本篇研究中，我們利用全細胞膜片鉗技術及鈣離子螢光影像，紀錄初代培養大鼠胚胎皮質神經元受 IL-1β 刺激時的電訊號與胞內鈣離子濃度 ([Ca2+]i) 的變化。實驗結果顯示 IL-1β (10 ng/mL) 顯著地增加了自發性興奮性突觸後電流 (EPSCs) 及動作電位的頻率。將細胞預處理 IL-1R1 阻斷劑，IL-1RA (1 ng/mL) 及 MyD88 抑制劑，ST2825 (10 μM)，則抑制了此頻率的增加。然而 IL-1β 處理並不影響神經細胞的靜止態維持電流 (holding current) 及靜止膜電位 (resting membrane potential);且對麩氨酸 (glutamate) 誘導的電流，亦無顯著影響。紀錄電流-電壓關係，IL-1β 可些微增加向內鈉離子電流，但不改變向外鉀離子電流。IL-1β 對電壓依賴型鈉離子通道 (Nav) 的失活態電壓 (inactivation voltage) 及從失活態恢復到活性態的時間 (recovery time) 也沒有影響。透過鈣離子螢光染劑 fura-2 紀錄 [Ca2+]i 的變化，我們發現 IL-1β濃度在 0.5-1μg/mL之間，皆可顯著地增加 [Ca2+]。 ST2825(10μM) 及 thapsigargin(3μM，使內質網鈣離子耗盡) 阻斷了此 [Ca2+]i 的增加。APV (100 μM) 與 DNQX (1 μM) 分別為 N-甲基-D-天門冬胺酸受體(NMDARs) 及 α-氨基-3-羥基-5-甲基-4-異惡唑丙酸受體 (AMPARs) 拮抗劑，處理細胞後，可抑制 IL-1β 引起的 [Ca2+]i 增加。此外，thapsigargin (3 μM) 的預處理同樣也抑制了 IL-1β 所誘導的 EPSCs 頻率上升。綜合這些結果我們認為 IL-1β 透過 IL-1R1–MyD88 訊息傳遞路徑，由胞內鈣庫釋放鈣離子，在不影響細胞膜離子通道活性狀況下，導致神經遞質釋放;透過神經突觸傳導，在神經之間正向回饋提升神經興奮性，增加 EPSCs 及動作電位的頻率。因此在神經發炎初期，尚未引起神經細胞程序性死亡機制時，IL-1β 濃度的上升，會使神經細胞更加容易興奮，進而影響神經傳導活性。 | zh_TW |
| dc.description.abstract | Interleukin-1β (IL-1β) is a proinflammatory cytokine and a hallmark of many neurologic disorders, including neurodegeneration. The canonical signaling pathway of IL-1β is to activate myeloid differentiation primary response 88 (MyD88) after the binding of IL-1β to its receptor (IL-1R1), activating NF-κB to transcript inflammatory-related genes. Most studies focused on the long-term effects of IL-1β on cellular activities. However, the immediate influence of IL-1β on neurotransmission is unclear. In this study, we applied the whole-cell patch clamp technique to record the electric activities and Ca2+ fluorescence imaging to monitor the changes in the intracellular Ca2+ concentration ([Ca2+]i) from the primary cultured rat embryonic cortical neurons under IL-1β treatment. Our results show that IL-1β (10 ng/mL) significantly increases the frequency of excitatory postsynaptic currents (EPSCs) and action potentials firing. Pretreating the cultured neurons with IL-1RA (1 ng/mL), an IL-1R1 antagonist, and ST2825 (10 μM), a MyD88 inhibitor, suppressed these increments in electric activities. However, IL-1β treatment did not affect the holding current, resting membrane potential, and glutamate-evoked currents. The current-voltage curve shows that IL-1β slightly and significantly increased the inward Na+ currents when depolarized to -20 mV from a holding potential of -70 mV, but did not change the outward K+ currents. The inactivation voltage and recovery time of the voltage-gated Na+ channels showed no difference after IL-1β treatment. We then loaded the cultured neurons with fura-2, a Ca2+-sensitive fluorescence dye, to monitor the changes in [Ca2+]i. IL-1β at 0.5-1 μg/mL could significantly elevate the [Ca2+]i. ST2825 (10 μM) and thapsigargin (3 μM, to deplete intracellular Ca2+ ER stores) blocked this elevation; blocking synaptic transmission by the N-methyl-D-aspartate receptors (NMDARs) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) antagonists, APV (100 μM) and DNQX (1 μM), respectively, also suppress this [Ca2+]i increment. Moreover, pretreating the cultured neurons with thapsigargin (3 μM) inhibited the enhancement effects of IL-1β on EPSCs frequency. These results demonstrate that IL-1β facilitates the excitability of neurons by releasing Ca2+ from ER Ca2+ stores via IL-1R1–MyD88 pathway without affecting the ion channels on the cell membrane. This elevation of [Ca2+]i triggers neurotransmitter release and enhances neuron excitability resulting in positive feedback among the cultured neurons through synaptic transmission. Therefore, at the early stage of neuroinflammation, before the activation of programmed cell death, the increase in the concentration of IL-1b will enhance the neuron excitability to regulate the excitability of neuronal circuits. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2023-08-09T16:44:26Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2023-08-09T16:44:26Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 致謝 i
中文摘要 ii Abstract iv Contents vi 1. Introduction 1 1.1 Cytokines 1 1.2 Interleukin-1β (IL-1β) 2 1.3 The signaling pathway, synthesis, and release of IL-1β 3 1.4 IL-1β in the central nervous system 7 1.5 The level of IL-1β concentration in the central nervous system 8 1.6 Glutamate receptors 9 1.7 Glutamatergic neurons and excitatory postsynaptic potential 11 1.8 Membrane potential and action potential 12 1.9 Voltage-gated ion channels in neurons 13 1.10 Endoplasmic reticulum Ca2+ stores 15 1.11 Mitochondrial Ca2+ stores 17 1.12 Neuronal Ca2+ signaling 18 1.13 IL-1β regulates LTP in the hippocampus 19 1.14 IL-1β regulates VGCCs and [Ca2+]i in the neurons 20 1.15 IL-1β regulates NMDA-induced [Ca2+]i elevation in the neurons 21 1.16 Aims 23 2. Materials and Methods 25 2.1 Chemicals 25 2.2 Primary cultured rat embryonic cortical neurons 25 2.3 Electrophysiology 27 2.4 Ca2+ imaging 30 2.5 Data analysis 31 3. Results 32 3.1 Differentiation of primary cultured rat embryonic cortical neurons 32 3.2 IL-1β increases the frequency of EPSCs through the IL-1R1–MyD88 pathway 32 3.3 IL-1RA and ST2825 do not affect the characteristics of EPSCs 33 3.4 IL-1α increases the frequency of EPSCs through the IL-1R1–MyD88 pathway 34 3.5 IL-1β has no apparent effect on the EPSC amplitude 35 3.6 IL-1β has no apparent effect on the ionotropic glutamate receptor 36 3.7 IL-1β increases the APs firing rate through IL-1R1–MyD88 pathway 37 3.8 IL-1β does not significantly affect the membrane potential at the resting state 38 3.9 IL-1β has no apparent effects on the voltage-dependent inward INa and outward IK 40 3.10 IL-1β has no apparent effect on the steady-state inactivation of Nav 41 3.11 IL-1β has no apparent effect on Nav recovery from inactivation 42 3.12 High concentration of IL-1β induced [Ca2+]i in a dose-dependent manner 43 3.13 Blocking the NMDA receptors inhibits the IL-1β-induced [Ca2+]i elevation 44 3.14 Blocking the AMPA receptors inhibits the IL-1β-induced [Ca2+]i elevation 45 3.15 APV and DNQX do not affect depolarization-evoked Ca2+ response 46 3.16 AMPA/NMDA receptor ratio in primary cultured cortical neurons 47 3.17 IL-1β-induced [Ca2+]i elevation via MyD88 signaling pathway 48 3.18 ST2825 does not affect the depolarization-evoked Ca2+ response 49 3.19 Depleting ER Ca2+ stores with Tg inhibits the IL-1β-induced [Ca2+]i elevation 50 3.20 Tg does not affect the depolarization-evoked Ca2+ response 51 3.21 Depleting ER Ca2+ stores with Tg inhibits the increment in EPSCs frequency induced by IL-1β 52 3.22 Tg does not affect the characteristics of EPSCs 53 4. Discussion 54 4.1 IL-1β regulates neurotransmission 55 4.2 IL-1β regulates neurotransmission via IL-1R1–MyD88 signaling pathway 57 4.3 IL-1β, voltage-independent ion channels, and membrane potential 58 4.4 IL-1β and voltage-dependent Na+ and K+ channels 61 4.5 IL-1β regulates [Ca2+]i level in a dose-dependent manner 64 4.6 IL-1β regulates [Ca2+]i via MyD88 signaling pathway 66 4.7 IL-1β, ER Ca2+ stores, and synaptic transmission 67 4.8 IL-1β, ER Ca2+ stores, and excitotoxicity 69 4.9 The physiological effect of IL-1β on the nervous system 70 Conclusion 73 References 74 Tables 98 Table 1 Characteristics of the EPSCs before and after mock or IL-1β treatment in the presence of inhibitors 98 Table 2 Characteristics of the basal EPSCs under IL-1RA or ST2825 pre-treatment 99 Table 3 Characteristics of the EPSCs before and after IL-1α treatment in the presence of inhibitors 100 Table 4 Characteristics of the APs before and after IL-1β treatment in the presence of inhibitors 101 Table 5 Glutamate-evoked inward current, holding current, and RMP before and after mock or IL-1β treatment 102 Table 6 Properties of Nav and Kv before and after mock or IL-1β treatment 103 Table 7 Characteristics of the EPSCs with APV and DNQX treatment 104 Table 8 The Δ Ratio (F340/F380) of Ca2+ responses with different drug treatment 105 Table 9 Characteristics of the EPSCs before and after IL-1β treatment in the presence of Tg 106 Figures 107 Fig. 1 The morphology of primary cultured rat embryonic cortical neurons at different days in vitro (DIVs). 107 Fig. 2 IL-1β increases the frequency of EPSCs through the IL-1R1–MyD88 pathway in cultured cortical neurons 109 Fig. 3 IL-1RA and ST2825 do not affect the characteristics of EPSCs in cultured cortical neurons 111 Fig. 4 IL-1α increases the frequency of EPSCs through the IL-1R1–MyD88 pathway in cultured cortical neurons 113 Fig. 5 IL-1β has no apparent effect on the EPSCs amplitude in cultured cortical neurons 115 Fig. 6 Glutamate-evoked inward current with mock treatment in cultured cortical neurons 117 Fig. 7 IL-1β has no apparent effects on glutamate-evoked inward current in cultured cortical neurons 119 Fig. 8 IL-1β increases the frequency of APs firing through the IL-1R1–MyD88 pathway in cultured cortical neurons 121 Fig. 9 IL-1β has no apparent effects on the holding current at –70 mV and RMP in cultured cortical neurons 123 Fig. 10 Local puff of IL-1β does not change the holding current at –70 mV in cultured cortical neurons 125 Fig. 11 Voltage-dependent-inward INa and outward IK current with mock treatment in cultured cortical neurons 127 Fig. 12 IL-1β has no apparent effects on the voltage-dependent inward INa and outward IK current in cultured cortical neurons 129 Fig. 13 IL-1β has no apparent effects on the steady-state inactivation of Nav in cultured cortical neurons 131 Fig. 14 IL-1β has no apparent effects on the Nav recovery from inactivation in cultured cortical neurons 133 Fig. 15 High concentration of IL-1β induces [Ca2+]i elevation in a dose-dependent manner in cultured cortical neurons 135 Fig. 16 Blocking NMDA receptor inhibits the IL-1β-induced [Ca2+]i elevation in cultured cortical neurons 137 Fig. 17 Blocking AMPA receptor inhibits the IL-1β-induced [Ca2+]i elevation in cultured cortical neurons 139 Fig. 18 KCl- and Glutamate-inducing [Ca2+]i elevation with APV and DNQX treatment in cultured cortical neurons 141 Fig. 19 AMPA/NMDA receptor ratio in primary cultured cortical neurons 143 Fig. 20 IL-1β induces [Ca2+]i elevation through MyD88 pathway in cultured cortical neurons 145 Fig. 21 KCl-inducing [Ca2+]i elevation with ST2825 treatment in cultured cortical neurons 147 Fig. 22 Depleting ER Ca2+ stores with Tg inhibits the IL-1β-induced [Ca2+]i elevation in cultured cortical neurons 149 Fig. 23 DHPG-inducing [Ca2+]i elevation with Tg treatment in cultured cortical neurons 151 Fig. 24 Depleting ER Ca2+ stores with Tg treatment inhibits the increment in EPSCs frequency induced by IL-1β in cultured cortical neurons 153 Fig. 25 Tg does not affect the characteristics of EPSCs in cultured cortical neurons 155 Fig. 26 Summary figure 157 | - |
| dc.language.iso | en | - |
| dc.subject | 胞內鈣庫 | zh_TW |
| dc.subject | 興奮性突觸後電流 | zh_TW |
| dc.subject | 電壓依賴型鈉離子通道 | zh_TW |
| dc.subject | 神經發炎 | zh_TW |
| dc.subject | 介白素-1β | zh_TW |
| dc.subject | 神經傳遞 | zh_TW |
| dc.subject | 骨髓分化初級反應蛋白 88 | zh_TW |
| dc.subject | voltage-gated Na+ channels | en |
| dc.subject | excitatory postsynaptic currents | en |
| dc.subject | interleukin-1β | en |
| dc.subject | intracellular Ca2+ stores | en |
| dc.subject | myeloid differentiation primary response 88 | en |
| dc.subject | neuroinflammation | en |
| dc.subject | neurotransmission | en |
| dc.title | 介白素-1β 於初代培養大鼠胚胎皮質神經元中透過 IL-1R1–MyD88 訊息傳遞路徑增強神經傳導 | zh_TW |
| dc.title | Interleukin-1β Enhances Neurotransmission via IL-1R1– MyD88 Signaling Pathway in Primary Cultured Rat Embryonic Cortical Neurons | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 111-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 張芳嘉;湯志永;江皓森 | zh_TW |
| dc.contributor.oralexamcommittee | Fang-Chia Chang;Chih-Yung Tang;Hao-Sen Chiang | en |
| dc.subject.keyword | 興奮性突觸後電流,介白素-1β,胞內鈣庫,骨髓分化初級反應蛋白 88,神經發炎,神經傳遞,電壓依賴型鈉離子通道, | zh_TW |
| dc.subject.keyword | excitatory postsynaptic currents,interleukin-1β,intracellular Ca2+ stores,myeloid differentiation primary response 88,neuroinflammation,neurotransmission,voltage-gated Na+ channels, | en |
| dc.relation.page | 157 | - |
| dc.identifier.doi | 10.6342/NTU202301985 | - |
| dc.rights.note | 同意授權(限校園內公開) | - |
| dc.date.accepted | 2023-07-26 | - |
| dc.contributor.author-college | 生命科學院 | - |
| dc.contributor.author-dept | 生命科學系 | - |
| dc.date.embargo-lift | 2028-07-24 | - |
| 顯示於系所單位： | 生命科學系 | |
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