| 研究生: |
萬昌鑫 Wan, Chang-Hsin |
|---|---|
| 論文名稱: |
多種受體在芝麻酚引起癲癇發作中扮演的角色 Roles of multiple and plastic receptors in sesamol-initiated seizures in mice |
| 指導教授: |
劉明毅
Liu, Ming-Yie |
| 學位類別: |
碩士 Master |
| 系所名稱: |
醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health |
| 論文出版年: | 2006 |
| 畢業學年度: | 94 |
| 語文別: | 中文 |
| 論文頁數: | 70 |
| 中文關鍵詞: | 癲癇 、N-甲基-D-天門冬氨酸鹽 、伽馬氨基丁酸 、芝麻酚 、發作 、菸鹼性乙醯膽鹼受體 |
| 外文關鍵詞: | r-aminobutyric acid, nicotinic acetylcholine receptors, seizure, sesamol, N-methyl-D-aspartate, epilepsy |
| 相關次數: | 點閱:90 下載:2 |
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當腦中腎上腺素受體、菸鹼性乙醯膽鹼受體、伽馬氨基丁酸受體或N-甲基-D-天門冬氨酸鹽受體被過度刺激後,會導致癲癇發作。本研究的目的是探討多種受體在芝麻酚引起癲癇發作中扮演的角色。初步的動物實驗中顯示,給予實驗小鼠芝麻酚,隨著劑量的增高,癲癇發作程度也隨之增高。使用雄性的BALB/c小鼠,給予腹腔注射芝麻酚300 mg/kg誘發癲癇發作,並記錄癲癇發作的程度計分以及痙攣到恢復的時間。在小鼠身上,分別使用各種受體增效劑或拮抗劑前處理,半小時後以觀察芝麻酚誘導癲癇發作並觀察紀錄。這些受體包含腎上腺素性受體 (α1、α2、β1和β2)、菸鹼性乙醯膽鹼受體、伽馬氨基丁酸A類、B類受體、α-氨基羥甲基噁唑丙酸受體和N-甲基-D-天門冬氨酸鹽受體。Prazosin (腎上腺素α1受體拮抗劑)、clonidine(腎上腺素α2受體增效劑)、yohimbine(腎上腺素α2受體拮抗劑)、mecamylamine(菸鹼性乙醯膽鹼受體拮抗劑)、muscimol(伽馬氨基丁酸A類受體增效劑)、baclofen(伽馬氨基丁酸B類受體增效劑)、NBQX(α-氨基羥甲基噁唑丙酸受體拮抗劑)和MK-801 (N-甲基-D-天門冬氨酸鹽受體拮抗劑)會增強芝麻酚引起的癲癇發作。結果顯示,芝麻酚引起癲癇發作的機制,和腎上腺素受體、菸鹼性乙醯膽鹼受體、伽馬氨基丁酸受體、α-氨基羥甲基噁唑丙酸受體或N-甲基-D-天門冬氨酸鹽受體可能有相關。
Overstimulation of noradrenergic neurons, nicotinic acetylcholine receptors (nAChR), γ-aminobutyric acid (GABA), or N-methyl-D-aspartate (NMDA) receptor in the brain results in seizures. The aim of this study was to investigate the roles of multiple receptors in sesamol-initiated seizures in mice. Our pilot data showed that sesamol induced seizures in a dose-dependent manner in mice. In this study, seizures were induced by sesamol (300 mg/kg, ip) administration, and then seizures score and duration of convulsion were recorded in male BALB/c mice. Agonists and antagonists of various receptors were administrated 30 min before sesamol-induced seizures. Noradrenergic (α1, α2, β1 and β2), nAChR, GABAA, GABAB, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA receptor were associ-ated with sesamol-induced seizures. Prazosin (noradrenergic α1 antagonist), clonidine (noradrenergic α2 agonist), yohimbine (noradrenergic β2 antago-nist), mecamylamine (nAChR antagonist), muscimol (GABAA agonist), ba-clofen (GABAB agonist), NBQX (AMPA antagonist) and MK-801 (NMDA antagonist) augmented sesamol-initiated seizures. It was suggested that noradrenergic receptors, nAChR, GABA, AMPA and NMDA receptors are involved in sesamol-induced seizures in mice.
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